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Small Bowel Resection – Indications, Contraindications

Small bowel resection is a commonly performed procedure in general surgery. The length of the small bowel allows for simple resection without significant compromise to the gastrointestinal (GI) system function in most situations. Familiarity with the bowel as well as the steps needed to perform a safe resection are key components of surgical training, even for those who do not specialize in GI surgery. This article will outline the basic steps in a small bowel resection, characterize certain situations requiring resection, and discuss the possible outcomes and complications associated with the procedure.

Anatomy and Physiology

The small bowel consists of 3 histologically sections: duodenum, jejunum, and ileum.

The duodenum is the most proximal segment, approximately 25 to 30 cm, extending from the pylorus. Its dual blood supply comes from the celiac axis and superior mesenteric artery (SMA). The gastroduodenal artery off the celiac axis branches into the anterosuperior and posterosuperior pancreaticoduodenal arteries which travel anterior and posterior to the duodenum and pancreatic head. These arteries form arcades with the anteroinferior and posteroinferior pancreaticoduodenal arteries which arise from the SMA.

The duodenum is further separated into 4 sequentially named portions. The first portion is the duodenal bulb. It is intraperitoneal and travels in a transverse rightward direction off of the pylorus. The second portion is the descending duodenum. It is retroperitoneal. This portion contains the ampulla of Vater (duct of Wirsung) and duct of Santorini. Its proximity to the biliary tree and pancreas make any surgical interventions in this portion uniquely challenging. The third portion is the transverse duodenum, and it is also retroperitoneal. Once the duodenum passes through the space between the aorta and SMA, it becomes the fourth portion, which turns upward after crossing midline. The ligament of Treitz is a thin muscular band that serves to connect the duodenum and jejunum to the surrounding connective tissue. This serves as the marker for the transition from the duodenum to the jejunum.

The jejunum is the second segment of the small bowel. It is approximately 100 cm long and is characterized anatomically by its circular muscular folds and long vasa recta providing blood supply. The jejunum is the maximum site for nutrient absorption except for B12, bile acids, and folate, which are absorbed in the ileum. Iron is also excluded, as it is absorbed primarily in the duodenum. Water and salt absorption almost primarily takes place in the jejunum.

The ileum is the final segment of the small bowel, encompassing the final 150 cm before meeting the cecum. It is characterized by its short vasa recta.

Blood supply for the jejunum and ileum comes from numerous branches coming off the SMA. There are roughly 5 to 6 jejunal branches and 6 to 8 ileal branches that form a highly redundant arcade of vessels, contained all within the small bowel mesentery. The terminal ileum and cecum received blood supply coming off the ileocolic artery. The ileocolic artery branches from the SMA separate from the ileal and jejunal branches, although shares branches with the prior. No watershed areas exist within a small bowel with healthy vasculature.

The surgical anatomy of the small bowel can be structurally separated into 3 layers: mucosa, muscularis, and serosal layers. In reality, there are several histologically distinct layers within the bowel wall with unique and important functions. These sublayers are indistinguishable to the naked eye though, and therefore not pertinent knowledge in the context of small bowel resection.

The innermost layer lining the lumen of the bowel is the mucosa. This consists of numerous folds of glandular epithelial tissue. It is richly vascularized with a high rate of tissue turnover and minimal strength for holding sutures. The submucosal nerve plexus makes up the outermost sublayer of the mucosa. Deep to this is the muscularis, with separate circular (inner) and longitudinal (outer) muscle separated by the myenteric nerve plexus. This layer primarily is responsible for mixing and propelling enteric contents through the bowel and has its own intrinsic basal electrical rhythm that controls peristalsis. Of note, the mucosa contains a thin band of the muscular mucosa, which has a minor effect on bowel motility. The outermost layers are the adventitia (for retroperitoneal structures) and serosa (additional layer for intraperitoneal structures). The adventitial tissue is largely fixed to surrounding retroperitoneal tissue, whereas serosa creates a clear boundary between the gut and surrounding tissue. The serosa connects to the mesentery along the inner wall of the bowel. These layers are composed of several layers of connective tissue and will provide an immobile strength layer to a small bowel anastomosis or when securing bowel to surrounding connective tissue.

Indications of Small Bowel Resection

There are many reasons for performing a small bowel resection (SBR), and common indications listed below. While the general principles of an SBR are nearly universal, modifications of the surgical technique may be required based on the pathology. Some common indications are listed below, with an abridged explanation of how each pathology needs to be specifically addressed.

  • Obstruction not amendable to adhesiolysis
  • Malignancy: Suspected malignancies will typically require 8-10 cm margins.
  • Non-traumatic perforation: The differential for adult patients includes ulcerative disease and malignancy. SBR may be preferred over the repair to allow for tissue diagnosis by a pathologist
  • Traumatic perforation: Defects can be repaired if they encompass less than 50% of the small bowel loop; otherwise, it will require resection.
  • Ischemic necrosis: This occurs secondary to emboli, thrombus, or low-flow malperfusion. Bowel ischemia is often progressive if the underlying diseases state is not corrected, requiring multiple resections over several days and carrying high morbidity
  • Inflammatory bowel disease (IBD): Resection is typically the last treatment choice reserved for strictures not amendable to stricturoplasty or conservative management. The inflammatory nature of IBD increases risk or complications
  • Enterocutaneous fistula not amendable to closure with conservative measures
  • Necrotizing enterocolitis with perforation
  • Symptomatic Meckel’s diverticulum or diverticular disease

Contraindications of Small Bowel Resection

There are no absolute contraindications that can be applied to the population in general. Active IBD is a relative contraindication, as local inflammation increases the risk of anastomotic leak. Few additional relative contraindications exist since SBR is usually only considered to remove a diseased segment without any additional therapeutic options.

Equipment

A standard laparotomy tray will typically contain all of the necessary instrumentation for an open SBR. Self-retaining table-mounted retractors such as the Omni-Flex or Bookwalter retractor systems can be helpful if the abdomen is to be explored. For a laparoscopic SBR, standard atraumatic graspers are preferred for handling the bowel to prevent iatrogenic serosal injury. Laparoscopic electrocautery or cutting devices such as the Ligasure or Harmonic Scalpel are required for mesenteric dissection.

Preparation

Small bowel resection can be done during an open or laparoscopic procedure depending on the timing and indication for the surgery. For elective resections, bowel preparation with a low residue diet for several days preceding the date of surgery is generally undertaken. Mechanical bowel prep may be added but is not standard. Conditions requiring SBR are often emergent and therefore pre-op planning is limited to supportive care for the critically ill patient.

The technique of Small bowel resection

SBR involving the ileum or jejunum is straightforward as long as the bowel is adequately mobile. Duodenal resections are exponentially more complex due to the duodenum’s retroperitoneal position and proximity of the Ampulla of Vater, biliary tree, and pancreas. For this reason, duodenal resections will almost always require an extra-anatomic reconstruction, often specific to the pathology being addressed. Given the variety and complexity of procedures to treat duodenal pathology and the marked difference between resecting duodenum versus the more distal bowel, it is reasonable to reserve discussion of those procedures for their specific pathologies. For the sake of this article, SBR will reference resection limited to the ileum or jejunum.

The entire small bowel should be examined before resection. If the surgery is being performed open, the portion being resected should be eviscerated and placed on a towel to limit contamination from spillage.

Resections are planned based on the intended anastomosis: stapled or hand sewn. For a stapled anastomosis, defects are made through the mesentery close to the bowel wall, away from large vessels. Gastrointestinal anastomosis staplers (GIA), usually 60 mm linear cutting with a soft tissue load, are placed across the bowel through the defects. Staplers are then fired at a slightly oblique angle above and below the diseased segment, cutting and sealing the bowel in unison. The diseased, isolated segment of bowel is then freed from the mesentery using electrocautery, with identified vessels suture ligated with silk suture. Once removed, the sealed ends are most commonly reconnected using a side-to-side, functional end-to-end anastomosis. In this technique, the proximal and distal segments are aligned in parallel with the mesenteric borders adjacent to one another. It is important to inspect the base of the mesentery to ensure there is no abnormal rotation of the tissue. Sero-muscular sutures should be placed on the mesenteric side for support and to prevent migration. Small enterotomies are then made on the anti-mesenteric corner each segment. A common channel is then created by placing one limb of a GIA stapler into each lumen through these enterotomies. Firing the stapler then creates a common channel between the 2 segments. The common channel should be inspected to ensure there is no intraluminal bleeding at the staple line. Once hemostasis is confirmed, the enterotomies are then closed, usually by exclusion by firing another TA or GIA stapler across the top of the anastomosis. Edges should be checked to ensure the serosa is incorporated into the staple line on both sides. As the corners of the staple line have the higher risk of ischemia, Lembert stitches using absorbable suture should be placed in the corners, allowing the tissue to invert beneath the suture. Lastly, the mesenteric defect is closed with permanent or absorbable suture to prevent internal herniation. Care must be taken to avoid strangulating the edges of the mesentery, as main blood flow to the anastomosis will come from this tissue.

A 2-layer, hand-sewn anastomosis will increase operative time but remains the preferred method for many surgeons. First, appropriate mesenteric defects are created. The mesenteric tissue between the 2 defects is then clamped, and suture ligated. Two non-crushing clamps are placed across the bowel at each of the desired locations of transection, and the bowel is divided sharply. A 1-cm stump should be left beyond the end of the clamps for suturing. Anastomoses will typically be done in an end-to-end fashion, however side-to-side and end-to-side methods can also be employed. The later can be especially useful when a size discrepancy exists between the 2 segments, such as when 1 segment is more distended and edematous, or when making an ileocecal anastomosis.

With the diseased bowel segment now cut and removed, the cut ends of the small bowel are held aligned and stay sutures are placed in the corners. The clamps holding the bowel ends are rotated in opposition to one another to bring the posterior outer serosal layers together. A series of silk interrupted Lembert sutures are then placed through the seromuscular layers to conjoin the 2 segments. This is continued until the stay sutures are reached at each end. Next, absorbable sutures are placed in full-thickness bites to form the posterior inner layer along the same distance. The sutures should be placed so that the mucosa inverts and contacts the opposing mucosa throughout. With the posterior layer complete, absorbable Connel (U-shaped) stitches are placed in the corner, and the pattern is continued to close the anterior inner layer. Suturing of the inner layers can be safely done with either interrupted or continuous patterns. Continuous sutures have shown in animal models to cause decreased perianastomotic tissue oxygen tension when compared to interrupted sutures; however, limited human trials have not shown any significant difference in anastomotic leak rates when comparing the 2. Once that anterior inner layer is closed, silk Lembert stitches are placed in interrupted fashion across the anterior outer surface, completing the 2-layer anastomosis.

If a single layer is preferred, the same steps as above are performed, with the Lembert stitches being excluded. A small bowel anastomosis can be safely created with single or double layer closure, largely depending on surgeon preference. Single layer closures have been shown to be faster when compared to a double layer. A Cochrane review concluded the 2 styles were equivocal in safety; however, a meta-analysis of available randomized trials comparing the 2 was only moderate quality, and therefore, the clinical discretion of the surgeon is always warranted. A single-layered closure is often preferred in patients with inherently narrow bowel lumens, such as neonates. A double-layer closure may cause a too-high risk of obstruction if the lumen is small. Overall, it is difficult to compare the 2 techniques on a broad scale, due to heterogeneity in all the factors that may affect the overall outcome. These factors include suture type, surgeon experience, patient factors such as disease being treated, and other comorbidities.

SBR that is done for mass or neoplasm will generally require oncologic margins of 8 to 10 cm along with associated mesentery and lymphatic tissue; whereas, benign processes only require limited resection with sparing of mesentery to preserve blood flow. If an oncologic resection is required, the primary vessel supplying the segment must be traced back to the mesenteric root and divided at its base. The adjacent mesentery is then fully resected in a wedge shape extending from the small bowel back to the origin of the vessel. This should allow for adequate lymph node harvest.

Under most circumstances surrounding a SBR, the surgeon will plan to return the small bowel to normal anatomic continuity. Numerous situations exist where this may not be preferred. The surgeon may opt for an extra-anatomic reconstruction if to bypass or exclude a segment of diseased or non-functional bowel that cannot otherwise be removed. With a distal ileum resection, creating of an ileocolonic anastomosis may be risky if there is a large size discrepancy between the two ends and/or a hostile environment from inflammation or infection. In this case, an end-ileostomy will be the safest option for the patient.

Creation of an ileostomy starts with choosing a site for the ostomy, away from other incision sites and above the belt line. When possible, this site should be chosen and marked pre-operatively with the patient awake and sitting upright. A circular segment of skin is excised at the chosen spot, and sharp dissection is used to create a passage through the subcutaneous tissue to the rectus sheath. The rectus sheath is incised, and the muscle is bluntly dissected down to the level of the peritoneum, which is entered sharply. With the distal ileum adequately mobilized, it is grasped with a Babcock and gently delivered through the stoma, along with its supporting mesentery. Care must be taken to keep the terminal ileum is its correct orientation. Once the ileum is through the stoma, the main abdominal incision should be closed and covered before opening the bowel. The stapled/sutured edge of the ileum should then be excised to produce a fresh bleeding edge. Absorbable sutures should be placed between the seromuscular layer of the bowel and the subcutaneous tissue in each quadrant to orient the ileostomy. Once secured, interrupted sutures can then be placed circumferentially, taking full-thickness bites of the bowel and securing it to the dermis. When tightened and tied, these should help to avert the end of the ostomy. Once complete, the ostomy should be checked for patency before application of a stoma appliance.

Complications

Superficial wound infections are common in contaminated cases. Allowing the wound to close by secondary intent can reduce the risk of soft tissue infection, abscess, and potential wound dehiscence.

Anastomotic breakdown or leak is the most feared common complication after SBR with incidence varying from 1% to 24% based on numerous factors. Risk can be reduced by focusing on operative technique to ensure adequate blood supply with minimal tension. This must be combined with appropriate preoperative and postoperative supportive care to mitigate the effects of systemic patient disease and prevent protein-calorie malnutrition.

Unlike high-risk colonic anastomoses that can be protected with the proximal diversion of the fecal stream, diversion is not an option in SBR. Proximal diversion of anything proximal to the terminal ileum would impair the guts absorptive function. Proximal decompression with a nasogastric or gastric tube can help alleviate early stress on the healing anastomosis. The anastomotic breakdown will inherently allow enteric contents to permeate into the peritoneal cavity, causing abscesses, peritonitis, and sepsis, and often progress to abdominal wound dehiscence.

Fistulization is a common subacute complication of anastomotic breakdown after SBR. Enterocutaneous fistulas are both a common sequelae of anastomotic leaks, as well as a common reason for additional SBR if they are persistent. Enteroenteric and enterocolonic fistulae are not uncommon findings in a hostile abdomen of a malnourished or hemodynamically impaired patient. These are likely under-recognized due to the lack of external clinical signs and can contribute to malabsorption by allowing enteric contents to bypass a variable portion of the small bowel’s absorptive surface.

SBR, as with any intraabdominal surgery, can contribute to adhesions which increase future risk for obstruction.[rx]

References

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Therapeutic Plasma Exchange – Indications, Contraindications

Therapeutic plasma exchange (TPE) is a procedure employed to “cleanse” the blood of various pathologic entities including antibodies, immune complexes, cellular elements, infectious agents, and toxins. A variety of conditions are responsive to therapy with TPE either as a first-line intervention or adjunct therapy. TPE, or plasmapheresis, consists of the separation of whole blood into its liquid and cellular components via centrifugal or membrane-filter technique followed by reintroduction of albumin and/or donor plasma tp the cellular components and re-infusion. This activity reviews the process of TPE, the evaluation and treatment of conditions responsive to therapeutic plasma exchange, and the role of an interprofessional team performing this interventional therapy.

Therapeutic plasma exchange (TPE) is a procedure in which blood or plasma is separated, removed, and replaced with a colloid solution of either albumin and/or donor plasma so as to accomplish the elimination of a pathologic entity.  Plasma is exchanged in volumes, usually between 1 to 1.5 L to remove dysfunctional cells, autoantibodies, immune complexes, cellular byproducts, parasites/bacteria, and toxins.  There are two different methods for plasma separation – manual and automated.

Plasma exchange is a therapeutic procedure used to treat a variety of diseases through the bulk removal of plasma. To apply this treatment to patients appropriately, it is essential to understand the methods to remove plasma, its effects on normal plasma constituents, the role of replacement fluids in the treatment, and the risks associated with the procedure. To facilitate the appropriate evidence-based use of plasma exchange and to encourage research, the American Society for Apheresis has published guidelines providing practical guidance and information to those responsible for ordering or providing this treatment.

Indications of Therapeutic Plasma Exchange

The American Society for Apheresis guidelines, Eight Edition, published in 2019, includes a periodically updated lengthy list of diseases with indications for TPE alone or along with other therapies.  It serves as a reference for TPE management of diseases, thoroughly detailing rationale, impact, technical issues, therapeutic plan, clinical/laboratory endpoints, and timing/location.  This summary is not nearly as inclusive or comprehensive as that reference, however, below are the most commonly encountered indications.

  • Sickle cell disease is an autosomal recessive group of inherited disorders affecting the production of the beta-globin subunits of hemoglobin.  Under episodes of physical insult (ie: hypo/hyperthermia, dehydration, emotional stress, hypoxia, etc) the red blood cells transform into a rigid sickled shape that does not easily traverse the vasculature. Sickle cells have abnormally short lifespans resulting in anemia in the affected individual. Additionally, patients suffering from sickle cell disease are also predisposed to certain bacterial infections and painful vaso-occlusive events known as sickle cell crisis, stroke, and death in addition to other comorbidities. Therapeutic plasma exchange is indicated for severe anemia and multiorgan failure.  The objective is to decrease vaso-occlusion by lowering the sickle hemoglobin to below 30% and raising the hemoglobin oxygen saturation.  At least one study has demonstrated that TPE has synergistic effects with red cell exchange therapy in patients with multi-organ failure.
  • Neonatal polycythemia is a neonatal condition whereby hematocrit (Hct) measures >65% in an infant born at term. It results from chromosomal anomalies, twin to twin transfusion syndrome, or growth restriction in the womb.  These infants are at risk of hyperviscosity and may develop symptoms of hypoglycemia, cyanosis, and apnea if not quickly managed with intravenous hydration.  Therapeutic plasma exchange is indicated for progressive symptoms refractory to initial treatment.  This must be initiated quickly as Hct peaks a few hours after birth.  In a systematic review and meta-analysis, it was found that crystalloid was as effective as a colloid in managing hematologic state by use of partial exchange transfusion.
  • Neonatal hyperbilirubinemia occurs when a neonatal born >35 weeks has a total bilirubin (TB) >25 mg/dL.  The causes are either physiologic (transient period of mismatched increased red blood cell production and bilirubin metabolism) or pathologic (a number of disease states involving immune-mediated hemolysis).  These infants are at risk for brain injury from bilirubin-induced neurologic dysfunction in which bilirubin crosses the blood-brain barrier and builds up within the tissue.  Phototherapy (PT) with ultraviolet light is the mainstay of therapy, however, TPE is indicated for persistently elevated TB levels despite PT.  Double-volume exchange transfusion will remove about 50% to 75% of TB from pre-exchange value.  Triple-volume exchange removes approximately 95% of TB but is rarely required.  Due to the prohibitive cost of even more advanced therapies such as intrauterine transfusion and immunoglobulin therapy, TPE is the primary alternative to phototherapy in the management of severe hyperbilirubinemia in the developing world.
  • Babesiosis is a disease caused by the parasite Babesia microti. It is carried and transmitted by the deer tick, Ixodes scapularis, and may also result from transmission from infected mother to fetus or infected blood product transfusion.  The parasite infects, replicates within, and destroys red blood cells resulting in hemolytic anemia and flu-like symptoms. The treatment regimen of atovaquone and azithromycin is often used for uncomplicated cases.  Severe cases involving end-organ damage (respiratory distress, sepsis, etc) may benefit from therapeutic plasma exchange – reducing parasite burden, correcting anemia, and removing inflammatory mediators and toxic by-products.
  • Guillain-Barre syndrome (GBS), or acute inflammatory demyelinating polyradiculoneuropathy, is an acute immune-mediated disorder targeting the myelin of the peripheral nervous system.  This is usually incited by antecedent bacterial or viral infections of the gastrointestinal or respiratory tract.  Initially, symptoms are numbness and weakness bilaterally starting in the distal extremities and progressing proximally.  GBS can become life-threatening if innervation of the cardiac and pulmonary systems is involved, or when severe chest wall skeletal muscle weakness develops.  Treatment is supportive measures along with intravenous immunoglobulins and TPE for severe cases.  The acute phase reactant, plasma fibrinogen, is elevated in acute GBS and its level is inversely related to treatment success.  Treatment with TPE is conducted until a continuous 30% decrease in plasma fibrinogen is observed.
  • Myasthenia gravis (MG) is an autoimmune disease characterized by chronic bilateral skeletal muscle weakness, particularly the ocular, oral, and facial muscles. Significant extremity weakness and respiratory muscle paralysis are usually affected only in cases of myasthenic crisis.  MG is caused by antibodies to the acetylcholinesterase (Ach) receptor at the terminal endplate of the neuromuscular junction. The consequence of diminished Ach activity due to inhibited and reduced Ach receptors accounts for the clinical presentation.  Treatment typically involves Ach inhibitors and immunosuppressants.  TPE removal of acetylcholine receptor antibodies is indicated for severe exacerbations involving bulbar dysfunction and/or respiratory compromise.  Treatment goals are short-term improvement in skeletal muscle strength and motor performance (neuromuscular junction transmission) as well as improvement in respiratory function.
  • Heparin-induced thrombocytopenia (HIT) is an anti-platelet antibody-mediated condition resulting in thrombocytopenia and thrombophilia. Heparin bound to the chemokine, platelet factor 4 (PF4), elicits an immune response directed against this structure.  The resulting complex of IgG, PF4, and heparin bind with and further activate platelets causing thrombi and thrombocytopenia. Initial treatment involves discontinuation of heparin.  Therapeutic plasma exchange is indicated in severe or persistent cases to remove such “HIT complexes”. A recent international practice survey revealed cardiovascular surgery followed by HIT-associated thrombosis as the most common reason to prophylactically treat re-exposures in patients requiring heparin.  The fluid replaced was often plasma and the occurrences of treatment were laboratory/clinical response-dependent.
  • Thrombotic thrombocytopenic purpura (TTP) is an autoantibody-mediated condition characterized by thrombophilia and thrombocytopenia. Often idiopathic, TTP’s mortality rate exceeds 90%, untreated. Antibodies crossreact against the ADAMTS13 enzyme, which catalyzes the degradation of von Willebrand factor (vWF).  When ADAMTS13 is inhibited, vWF’s action is unopposed and thrombophilia results.  Symptoms include diffuse ecchymosis and petechiae, jaundice, fever, weakness, headaches, confusion, tachycardia, and tachypnea.  TPE is employed to remove IgG and resupply with functional ADAMTS13. Plasma exchange is more effective than plasma infusion.  TPE is conducted daily until levels of lactate dehydrogenase (which increases in thrombophilic conditions) and platelets normalize.
  • Goodpasture syndrome (GPS) or anti-glomerular basement membrane disease is an idiopathic, autoimmune disease directed against the basement membrane (alpha-3-subunit of type IV collagen) in tissues unique to lungs and kidneys. Symptoms typically consist of chest pain, shortness of breath, hemoptysis, and hematuria. Mortality is high without proper diagnosis and intervention.  Treatment with immunosuppressants and TPE reduces renal and pulmonary injury and provides symptom relief. The anti-GBMs promptly decrease with TPE and immunosuppression, thus serving as an effective marker to guide ongoing therapy.
  • Renal transplant is yet another application of TPE. It is indicated prior to, during, and after transplantation. TPE aids in the desensitization of the immune system and to remove antibodies that damage renal vasculature following transplant and potentially result in rejection.
  • Malaria is a disease caused by several species of the Plasmodium parasite, typically transmitted via the Anopheles mosquito. Once in the bloodstream the parasite infects and destroys liver cells and red blood cells.  Severe flu-like symptoms of fluctuating shivers and sweats, diffuse body pain, and weakness accompanied by jaundice and respiratory distress are the disease hallmarks. Death is not uncommon. Treatment with antimalarial medications (often artemisinin-combination therapy) is typically effective in uncomplicated cases.  Though not endorsed by the World Health Organization or the United States Centers for Disease Control and Prevention, TPE is occasionally used.  One retrospective study found mixed results with TPE in observed physiologic improvements (liver functions and inflammatory markers) but no improvement in parasite burden or disease state.

Equipment of Therapeutic Plasma Exchange

Intravenous access (needles, catheters, tubing, etc) for two sites on the body, centrifuge (speeds of 2000-2500 rpm), or plasma separation filter (60 to 900 kDa = albumin to IgM), anticoagulant (citrate or heparin), and replacement fluid (albumin or fresh frozen plasma).

Personnel

The individuals necessary for the performance of TPE are the pheresis technician, pathologist, and hematologist beyond the treating physician. Contact and communication between these individuals are vital to the expeditious treatment of each patient.

Preparation

To assure blood product safety, several measures require implementation during product collection, manufacturing, and storage. The World Health Organization has supported a global initiative to improve access to safe and sufficient blood supply. Once collected, the blood is tested for donor blood type and screened for any clinically significant donor antibodies. The collecting facility typically holds the blood until the appropriate preparation and routine screening for potential transfusion-transmitted infections is complete.  When all legal and industry standards have been met and the product is ready for transfusion, then it is “labeled” (i.e. identified as ready for use).

Widespread prioritization of testing for transfusion-transmitted infections has improved blood product safety worldwide. There is a summary of information on countries that responded to questionnaires about their particular policies and guidelines surrounding the testing of donor blood in Figure 2 according to the World Health Organization 2016 Global Status Report on Blood Safety and Availability report. The survey found that the majority of responding countries had policies for testing the most common and clinically relevant transfusion-transmitted infections including HIV, hepatitis C, hepatitis B, and syphilis. Eighteen nations in Latin America reported having a policy for testing all blood donations for Trypanosoma cruzi along with twelve countries implementing selective testing for T cruzi in donors who have traveled to high-risk areas or have defined risk factors. Thirty-seven nations reported having a policy of testing all blood donations for antibody to human T-lymphotropic virus (HTLV-I/II) along with seven countries reporting selective additional testing for new donors.

Following the collection of a blood donation, several procedures can take place during the preparation of blood for transfusion. Leukodepletion is a procedure to reduce the number of white blood cells in a blood product to reduce the risk of febrile reactions, HLA sensitization, and CMV transmission. Bacterial contamination testing of platelets can be performed prior to transfusion to avoid septic transfusion reactions. Plasma fractionation provides the opportunity to derive specific factors concentrates and intravenous immune globulin.  Gamma irradiation of blood products can be performed to reduce the risk of transfusion-associated graft-versus-host disease, which is nearly always fatal. Plasma reduction or washing of blood products limits the amount of plasma within a cellular blood product, which reduces the risk of allergic transfusion reactions or the effects of incompatible ABO antibodies.  Volume reduction can also be used to reduce excess potassium and cytokines which can cause electrolyte imbalance and febrile non-hemolytic transfusion reactions, respectively. Blood typing and screening for donor and recipient alloantibodies as well as compatibility testing are also important aspects of preparation for transfusion.  Screening the donated blood for alloantibodies is essential in the prevention of hemolytic transfusion reactions in recipients.

The new frontier in blood product safety is pathogen reduction (pathogen inactivation) which is a broad term for various methodologies applied to blood products post-collection to reduce the risk of transmission of infectious agents. Many of these technologies confer protection across different classes of infectious agents including viruses, bacteria, and parasites. Another potential benefit is that some of these technologies also inactivate donor white blood cells, which has allowed some to gain approval for the prevention of transfusion-associated graft-versus-host disease (as an alternative to irradiation). Pathogen reduction procedures are currently approved in some countries for platelets and plasma. These novel technologies can increase the shelf life of platelets and decrease the incidence of adverse transfusion reactions and bacterial contamination. These approaches are increasingly common in practice and should help improve blood product safety profiles.

Technique of Therapeutic Plasma Exchange

Centrifugal therapeutic plasma exchange: A continuous flow extracorporeal circuit is formed from the patient to the centrifuge and back to the patient. Citrate (anticoagulant) is added to the blood flow of 10-150 ml/min, while centrifugal forces separate and sieve off plasma from the heavier (white and red cells) of blood.  A replacement fluid (albumin and/or fresh frozen plasma) is recombined with the blood and returned to the patient.

Membrane therapeutic plasma exchange: A continuous flow extracorporeal circuit is formed from the patient to the filter-membrane and back to the patient. Heparin (anticoagulant) is added to the blood flow of 150 ml/min while membrane ultrafiltration properties of pore size and distribution separate and sieve off plasma from the heavier (white and red cells) of blood.  A replacement fluid (albumin and/or fresh frozen plasma) is recombined with the blood and returned to the patient.

An important aspect of the donation process is the donor screening questionnaire. Donor recruitment represents an essential front-line mechanism for ensuring blood safety. The highest rates of transfusion-transmitted infections are present among donors receiving monetary compensation, and conversely, the lowest rates of infection are among unpaid volunteer donors.   “Replacement” and “family” donors are relied on in some countries, but these are not considered as safe as true altruistic unpaid volunteers.  A great reduction in the risk of transfusion-transmitted HIV, HCV, HBV, and syphilis infections have transpired with the initial donor screening questions and improved testing, including serology and nucleic acid amplification testing. According to the United States, Food and Drug Administration, highly sensitive donor screening questionnaires designed to defer high-risk donors for infection transmission exclude an estimated 90% of potentially infectious donors from blood donation.  Donors that have incentives to donate (such as monetary gain or wanting to help a friend) may not be completely truthful during screening.

Individual blood service organizations may have subtle variations in collection procedures, but the World Health Organization provides guidelines on the proper technique for venipuncture for blood donation.  These standardize the process and are in place to prevent transfusion-transmitted infections. A safe collection is paramount to ensure that blood products remain safe through the collection, storage, and transfusion.

Bacterial contaminants typically come from normal skin flora; therefore, proper antiseptic technique before the collection is required. The recommended procedure by the World Health Organization includes the application of a combination 2% chlorhexidine gluconate and 70% isopropyl alcohol for 30 seconds followed by 30 seconds drying time.  A closed collection system (not open to the air) is used to ensure sterility.   This procedure means that the anticoagulant-containing collection bag has an intrinsically attached tube and needle. The first 15 to 20 mL of blood is collected in a diversion bag so that, in the case of possible skin contamination, the initial blood collected is used for laboratory testing and not transfused. This diverted blood is the most likely to be contaminated by skin flora and the skin plug (created by the needle), therefore removing this from the transfusion reduces contamination risk.  Blood volumes collected vary by the technique used. According to the World Health Organization, generally for whole blood transfusion, 350 milliliters of blood is collected, and for double or triple bags to make packed red cells, fresh frozen plasma, and platelet concentrations, a volume of 450 milliliters is necessary. The volume is selected to prevent donor transfusion-associated anemia and other adverse events.

Blood donations can be separated into four main components (red blood cells, platelets, plasma, and cryoprecipitate) or left as whole blood. Once the blood has undergone processing, it is stored at appropriate temperatures (often +2 C to +6 C).  Platelets and fresh frozen plasma (FFP) require preparation within 8 hours of collection. Platelets are stored at room temperature and with agitation typically for five days unless additional shelf life-extending mechanisms are employed.  Depending on the national regulations, fresh frozen plasma can remain stored at −18 C for one year, −25 C for 36 months, or at −65 C for seven years.   Many countries are moving toward making “plasma” instead of FFP, which gives them up to 24 hours after collection before processing and freezing are required.  The temperature and duration of storage depend on blood service guidelines and storage capabilities of individual institutions. Sterility is maintained during processing and storage steps to avoid contamination. Blood units are unavailable for transfusion until undergoing appropriate testing, including ABO and Rh blood group typing and antibody screening, as well as serologic testing for transfusion-transmitted infections.

Function

Red Blood Cells

The literature strongly supports adhering to a restrictive transfusion strategy (7 g/dL) in hospitalized adult and pediatric intensive care patients who are hemodynamically stable. The evidence is not as compelling for patients with cardiovascular disease, but recommendations are to adhere to a restrictive strategy (hemoglobin 8 gm/dL) for patients with preexisting cardiovascular disease. There is insufficient evidence to make recommendations for patients with the acute coronary syndrome.

RBC transfusion is indicated in actively bleeding patients. The amount should be based on clinical assessment and, if possible, by laboratory tests to guide targeted therapy. However, in patients with upper gastrointestinal bleeding, patients with a restrictive transfusion strategy may have better outcomes.

Plasma

There is minimal guidance for plasma transfusion. However, plasma is a frequently prescribed intervention, often for mild to moderate elevations in prothrombin time or an international normalized ratio (INR). This continues to occur despite numerous studies that failed to show a relationship between these elevations and the risk of bleeding or that INR has any ability to predict bleeding.

The Cochrane Reviews found no evidence to support plasma transfusions in patients who were not coagulopathic undergoing elective cardiac surgery or critically ill patients.

The British Society of Haematology (BSH) published recommendations in 2018 for various patient groups in the absence of major bleeding.

  • There is no evidence to support the prophylactic use of plasma in non-bleeding patients with abnormal standard coagulation tests pre-procedure
  • The impact of commonly used doses to correct clotting results or to reduce the bleeding risk is very limited, especially when the PT ratio or INR is between 1.5 to 1.9.
  • Vitamin K should be administered in patients with prolonged PT that is likely to be due to acquired vitamin K deficiency.

In patients with liver disease, plasma is often transfused to correct a prolonged INR. British Society of Haematology recommends these guidelines:

  • PT and APTT do not reflect the true hemostatic status of patients with advanced liver disease.
  • There is no good evidence to endorse the use of prophylactic plasma for correction of abnormal clotting tests in non-bleeding patients prior to interventions such as elective variceal bleeding.
  • There is no good evidence to support a role for prophylactic plasma to reduce the risk of bleeding from a percutaneous liver biopsy.
  • Prophylactic transfusion of plasma should not be given in low bleeding risk procedures.
  • Do not use plasma for volume replacement.

And for sites that have 4-Factor Prothrombin Concentrates such as K-Centra and Bebulin, this should always be the first therapeutic of choice to reverse warfarin emergently.

Cryoprecipitate

There are little data on the use of cryoprecipitate in non-bleeding patients, and it is often used prophylactically but not based on good quality evidence.

The British Society of Haematology recommends:

  • There is insufficient evidence on which to base a recommendation about the threshold of fibrinogen to transfuse cryoprecipitate, or the optimal dose, in patients with hypofibrinogenemia undergoing procedures.
  • If fibrinogen is <1.0g/L (100 mg/dL) and other factors (i.e., personal/family bleeding history, drug history, bleeding risk associated with planned procedure) indicate a significant bleeding risk before a procedure, a starting dose of two five donor pools of cryoprecipitate [10 individual units] can be considered (but there is no evidence to support this).

Many US sites consider fibrinogen <2.0 g/L (<200 mg/dL) in a bleeding obstetric patient as an indication to transfuse cryoprecipitate.

Platelets

Common guidelines for platelet transfusions include:

  • Prophylaxis against bleeding—PLT count <10,000 mg/dL
  • Neonate—PLT count <50,000 mg/dL
  • Bedside procedure—PLT count <50,000 mg/dL
  • Kidney or liver biopsy—PLT count <50,000 mg/dL
  • Bronchoscopy without biopsy—PLT count <50,000 mg/dL
  • Bronchoscopy with biopsy—PLT count <75,000 mg/dL
  • Intra-/postoperative bleeding—PLT count <50,000 mg/dL
Clinical bleeding with dysfunctional PLTs
  • PLT count <50,000 mg/dL (medical)
  • PLT count <100,000 mg/dL (surgical
  • Neurosurgery—PLT count <100,000 mg/dL

Cell Salvage

The Association of Anaesthetists guidelines make the following transfusion recommendations: Use cell salvage when it can be expected to reduce the likelihood of allogeneic (donor) red cell transfusion and/or severe postoperative anemia. Collection of blood for potential cell salvage (‘collect only’ mode) should be considered for surgical procedures where blood loss may exceed 500 ml (or > 10% of calculated total blood volume) in adult patients or > 8 mL/kg (> 10% of calculated total blood volume) in children weighing > 10 kg.

Whole Blood

There has been increasing interest in using low titer group O whole blood (LTOWB) in military and civilian trauma, and there is evidence to show that it saves lives.  It has also been used in non-trauma massive hemorrhage cases. LTOWB provides all of the components of blood (RBCs, platelets, and plasma with fibrinogen) and provides a balanced resuscitation addressing oxygen needs and coagulopathy in a single bag of blood. The whole blood has a critical titer of anti-A and anti-B of less than 50 to 200). The transfusion of up to 4 units of whole blood has been shown to be safe.

Complications

There are multiple complications of blood transfusions, including infections, hemolytic reactions, allergic reactions, transfusion-related lung injury (TRALI), transfusion-associated circulatory overload, and electrolyte imbalance.

According to the American Association of Blood Banks (AABB), febrile reactions are the most common, followed by transfusion-associated circulatory overload, allergic reaction, TRALI, hepatitis C viral infection, hepatitis B viral infection, human immunodeficiency virus (HIV) infection, and fatal hemolysis which is extremely rare, only occurring almost 1 in 2 million transfused units of RBC.

Adverse Event And Approximate Risk Per Unit Transfusion Of RBC

  • Febrile reaction: 1:60
  • Transfusion-associated circulatory overload: 1:100
  • Allergic reaction: 1:250
  • TRALI: 1:12,000
  • Hepatitis C infection: 1:1,149,000
  • Human immunodeficiency virus infection: 1:1,467,000
  • Fatal hemolysis: 1:1,972,000

Febrile reactions are the most common transfusion adverse event. Transfusing with leukocyte-reduced blood products, which most blood products in the United States are, may help reduce febrile reactions. If this occurs, the transfusion should be halted, and the patient evaluated, as a hemolytic reaction can initially appear similar and consider performing a hemolytic or infectious workup. The treatment is with acetaminophen and, if needed, diphenhydramine for symptomatic control. After treatment and exclusion of other causes, the transfusion can be resumed at a slower rate.

Transfusion-associated circulatory overload is characterized by respiratory distress secondary to cardiogenic pulmonary edema. This reaction is most common in patients who are already in a fluid overloaded state, such as congestive heart failure or acute renal failure. Diagnosis is based on symptom onset within 6 to 12 hours of receiving a transfusion, clinical evidence of fluid overload, pulmonary edema, elevated brain natriuretic peptide, and response to diuretics.

Preventive efforts, as well as treatment, including limiting the number of transfusions to the lowest amount necessary, transfusing over the slowest possible time, and administering diuretics before or between transfusions.

Allergic reaction, often manifested as urticaria and pruritis, occurs in less than 1% of transfusions. More severe symptoms, such as bronchospasm, wheezing, and anaphylaxis are rare. Allergic reactions may be seen in patients who are IgA deficient as exposure to IgA in donor products can cause a severe anaphylactoid reaction. This can be avoided by washing the plasma from the cells prior to transfusion. Mild symptoms, such as pruritis and urticaria can be treated with antihistamines. More severe symptoms can be treated with bronchodilators, steroids, and epinephrine.

Transfusion-related lung injury (TRALI) is uncommon, occurring in about 1:12,000 transfusion. Patients will develop symptoms within 2 to 4 hours after receiving a transfusion. Patients will develop acute hypoxemic respiratory distress, similar to acute respiratory distress syndrome (ARDS). Patients will have pulmonary edema without evidence of left heart failure, normal CVP. Diagnosis is made based on a history of recent transfusion, chest x-ray with diffuse patchy infiltrates, and the exclusion of other etiologies. While there is a 10% mortality, the remaining 90% will resolve within 96 hours with supportive care only.

Infections are a potential complication. The risk of infections has been decreased due to the screening of potential donors so that hepatitis C and human immunodeficiency virus risk are less than 1 in a million. Bacterial infection can also occur, but does so rarely, about once in every 250,000 units of red cells transfused.

Fatal hemolysis is extremely rare, occurring only in 1 out of nearly 2 million transfusions. It is the result of ABO incompatibility, and the recipient’s antibodies recognize and induce hemolysis in the donor’s transfused cells. Patients will develop an acute onset of fevers and chills, low back pain, flushing, dyspnea as well as becoming tachycardic and going into shock. Treatment is to stop the transfusion, leave the IV in place, intravenous fluids with normal saline, keeping urine output greater than 100 mL/hour, diuretics may also be needed, and cardiorespiratory support as appropriate. A hemolytic workup should also be performed which includes sending the donor blood and tubing as well as post-transfusion labs (see below for list) from the recipient to the blood bank.

  • Retype and crossmatch
  • Direct and indirect Coombs tests
  • Complete blood count (CBC), creatinine, PT, and PTT (draw from the other arm)
  • Peripheral smear
  • Haptoglobin, indirect bilirubin, LDH, plasma free hemoglobin
  • Urinalysis for hemoglobin

Electrolyte abnormalities can also occur, although these are rare, and more likely associated with large volume transfusion.

  • Hypocalcemia can result as citrate, an anticoagulant in blood products binds with calcium.
  • Hyperkalemia can occur from the release of potassium from cells during storage. Higher risk in neonates and patients with renal insufficiency.
  • Hypokalemia can result as a result of alkalinization of the blood as citrate is converted to bicarbonate by the liver in patients with normal hepatic function.

Transfusion Reactions

Transfusion reactions that can occur with the transfusion of blood range from life-threatening reactions to circumstances in which transfusion can continue, once the cause of the reaction is determined (e.g. simple allergic reaction).  The most common reactions include the following:

  • Transfusion-associated circulatory overload (TACO)
  • Transfusion-related acute lung injury (TRALI)
  • Transfusion-associated dyspnea (TAD)
  • Simple allergic reaction
  • Anaphylactic reaction
  • Hypotensive transfusion reaction
  • Febrile non-hemolytic transfusion reaction (FNHTR)
  • Acute hemolytic transfusion reaction (AHTR)
  • Delayed hemolytic transfusion reaction (DHTR)
  • Delayed serologic transfusion reaction (DSTR)
  • Transfusion-associated graft vs. host disease (GVHD)
  • Post-transfusion purpura (PTP)
  • Transfusion-transmitted infection (TTI)

References

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Platelet Transfusion – Indications, Contraindications

Platelet transfusion is a lifesaving procedure that is carried out to prevent bleeding or stop ongoing bleeding in patients with low platelet count or functional platelet disorders. There are minimum thresholds at which platelets are transfused in these patients, as not all low levels of platelet warrants a transfusion. Platelet is a scarce resource as processing, preparing, and transfusing it requires a great deal of precision and effort to maintain a certain quality. This activity highlights the use of platelet transfusion by the interprofessional team.

Since the first attempted blood transfusion in the 17th century, blood transfusion has evolved from transfusing whole blood to utilizing only its components for select indications such as packed red blood cells (RBC), platelets, rarely white blood cells (WBC), frozen plasma and plasma-derived products. Platelets play an integral role in hemostasis by its response to vascular injury. The relevance of platelet component therapy was better understood in the 1950s and 1960s when severe and fatal hemorrhagic complications of chemotherapy in leukemia were studied.

In the middle of the last century, blood was collected in glass bottles, which depleted platelets on storage. Around the same time introduction of plastic bags revolutionized blood storage. It was also found to be gas permeable, which is essential for storing functional platelet. Over time, with the development of efficient separation techniques, platelet component with high platelet yield has been achieved with apheresis, changes in safety protocol reduced adverse outcomes of transfusions. A great deal has been done to minimize adverse outcomes, and further safety protocols are being explored.

Platelet concentrates (PC) are widely used to support patients with severe thrombocytopenia. These could be patients with hematologic malignancy, bone marrow failure, or other immune and non-immune causes of platelet destruction, though rare cases could warrant transfusion with normal platelet counts. Platelet is a scarce resource, partly because of its short shelf life of 5 days; it is classified in the World Health Organization’s (WHO) list of “Essential Medicine.”

Anatomy and Physiology

Platelets are anucleated discoid cells, size averaging between 2.0 to 5.0 micrometers in diameter, 0.5 micrometers in thickness with a mean cell volume of 6 to 10 femtoliters. Platelets are produced in the bone marrow through megakaryopoiesis from a hematopoietic stem cell (HSC) under the influence of thrombopoietin and appropriate growth factors, and an estimated ten thousand platelets are pumped into the circulation every single day. It has a life span of 8 to 10 days, after which structural changes on its surface are recognized by the liver where these senescent platelets are cleared from the circulation.

Platelets are primarily involved in the hemostasis by adhesion to the disrupted endothelium, secretion of mediators from its granules which promote aggregation, coagulation (by providing a surface to a host of proteins) and finally the clot retraction by the action of contractile proteins in the platelet together with its secretions and entrapped mesh of fibrin. Other roles played by platelet in the body include participation in inflammation, mitogenesis, wound healing, and antimicrobial host deficiencies.

Structurally a platelet is divided into three zones:

  • Peripheral zone – this zone is primarily involved in adhesion and aggregation function
    1. Glycocalyx – This is the thick carbohydrate-rich structure found on the exterior surface of platelets and serves as the site of the first contact during the hemostatic response by platelets, and it is made up of major and minor glycoproteins. GP-Ib-IX-V complex involved in adhesion at site of vascular injury. GPIIb-IIIa is involved in aggregation by attachment through fibrinogen to other platelets.
    2. Unit membrane – It is made of a lipid bilayer and open canalicular system, which serves a vital role in the acceleration of coagulation through the anionic phospholipid, phosphatidylserine, provided by the surface of activated platelets when clotting is initiated which converts prothrombin to thrombin.
    3. The submembrane area – It plays a vital role in transmitting signals from the surface to organelles in the cytoplasm regulating signal processes of platelet activation.
  • Sol-gel zone – This is the matrix that is made of microtubules and microfilament, which plays a vital role in platelet structure and its support. This zone is responsible for various shape changes on activation during hemostasis and during ex vivo storage. Organelles are embedded within this matrix.
  • Organelle zone
    • Alpha-granules which stores fibrinogen fibronectin FV vWF, PDGF cytokines, chemokines, TG-beta-1 and VEGF
    • Dense- granules stores calcium ATP, ADP, serotonin, and pyrophosphate
    • Mitochondria- Are the powerhouse of platelets
    • Glycogen
    • Lysosome and peroxisome

When a platelet is activated, secretions from the α and dense granules are involved in further platelet activation and aggregation. Secretions also have immune-mediated effects.

Indications

Normal platelet count in humans ranges from 150,000 to 450,000 cells/microliter. Platelet transfusion is mainly indicated to treat or prevent bleeding in patients with thrombocytopenia or platelet function disorder.

Platelet transfusion Threshold in Bleeding Patients

  • <50,000 cells/microliter in severe bleeding including disseminated intravascular coagulation (DIC)
  • <30,000 cells/microliter when bleeding, not life-threatening or considered not severe
  • <100,000 cells/microliter for bleeding in multiple trauma patients or patients with intracranial bleed.

Prophylactic Transfusion Threshold

Prophylactic platelet transfusion is indicated below a specific threshold and is indicated before specific procedures or to prevent spontaneous bleeding. These include the following:

  • To prevent spontaneous bleeding – transfuse at <10,000 cells/microliter, some recommend <5,000 cells/microliter
  • Before neurosurgery or ocular surgery – <100,000 cells/microliter
  • Before major surgery – <50,000 cells/microliter
  • In DIC – <50,000 cells/microliter
  • Before central line placement – <20,000 cells/microliter
  • Before epidural anesthesia – <80,000 cells/microliter
  • Before bronchoalveolar lavage (BAL) – 20,000 to 30,000 cells/microliter
  • Before endoscopic procedures – <50,000 cells/microliter for therapeutic procedures; <20,000 cells/microliter for low-risk diagnostic procedures
  • Vaginal delivery platelet transfusion is considered at <30,000 cells/microliter, and when traumatic delivery then <50,000 cells/microliter.
  • Before lumbar puncture – <20,000 cells/microliter in patients with hematologic malignancies and 40,000 to 50,000 cells/microliter in patients without hematologic malignancies
  • Platelet transfusion is not routinely indicated prior to bone marrow biopsy, peripheral, central catheter insertion, traction removal of tunneled central venous catheters, and cataract removal.

Platelet Transfusion in Specific Settings

  • Idiopathic thrombocytopenic purpura (ITP) – transfusion is avoided unless severe bleeding is present.
  • Malignancy and chemotherapy – In most cancers, platelet transfusion thresholds are as indicated above except in acute promyelocytic leukemia in which there is increased bleeding risk. Hence transfusion is indicated at counts <30,000 cells/microliter. chemotherapy is carried out at counts >20,000 cells/microliter.
  • Cardiac surgery – Patients undergoing cardiac surgery get exposed to a blood-pumping circuit, which activates platelets that get destroyed once back in circulation; hence even at normal counts, platelet transfusion is indicated during cardiac surgery.
  • Inherited and acquired platelet disorders like Glanzmann thrombasthenia, Bernard-Soulier syndrome, and other congenital platelet defects, acquired platelet disorders like patients with uremia or drug-induced platelet dysfunction. In these situations, platelet transfusion is indicated only when bleeding Is present.
  • For pediatric patients, transfusion indications are otherwise similar in older infants and children compared to adults, as demonstrated by the PLADO study except in the following situation. We transfuse platelets when the platelet count is:
    • <30,000 cells/microliter in neonates without any bleeding or symptom and failure to produce platelet.
    • <50,000 cells/microliter in an infant with active bleed or undergoing an invasive procedure. For the same situation in a premature infant, we transfuse at <100,000 cells/microliter.
    • Patient undergoing extracorporeal membrane oxygenation (ECMO) and platelets <100,000 cells/microliter

Contraindications

The only agreed upon contraindication to platelet transfusion is thrombotic thrombocytopenic purpura (TTP) due to increased risk of thrombosis, although studies on outcomes and mortality have shown mixed results. Platelet transfusion is reserved for life-threatening bleeding only.

Heparin-induced thrombocytopenia (HIT) is another condition where platelet transfusion may increase the risk of thrombosis, but recent studies have shown no risk association. In HIT, transfusion is reserved only for pre-procedure or surgery, and in severe bleeding, prophylactic transfusion, however, is not indicated.

Equipment

Platelets are transfused at the bedside through intravenous tubing with an in-line filter (screen filter of 170-260 micrometer pore size) to remove fibrin clots and large debris. The tubing can be primed with normal saline or blood product itself.

Emergency equipment as 0.9% normal saline, oxygen source, and emergency medication to treat anaphylaxis should be available at hand in case of transfusion reaction.

Personnel

This involves multidisciplinary departments from clinicians to ancillary medical services. Platelet to be transfused is to be ordered by the physician and administered by the transfusions, which can be a nurse, who verifies the identity of the patient and match the unit before transfusing.

Preparation

Preparation for platelet transfusion starts from the production of quality approved platelet concentrates (PC) in the blood banks. PC can be prepared from whole blood or by apheresis. 6 whole blood unit derived platelets equal one apheresis platelet which contains 3X10 platelets per unit, the shelf life of PC is five days within which it must be used. The normal dose of platelet transfused is calculated as 10 to 15 ml/kg of the patient.

The blood bank receives a request for transfusion from the physician with a pretransfusion sample, which is verified by the staff at both ends, following which ABO and Rh blood grouping is confirmed. PC is issued as and when required, which is mentioned on the blood request form. Group-specific PC is recommended, although out of the group can also be issued. When an emergency request for platelet transfusion is made, such as in traumatic bleeding patients, the patient blood group may not be available. In such cases, “AB” group platelets are given if available or else across the group transfusion is considered. Serologic crossmatch is not required except in rare cases where PC have high RBC content.

Consent from the patient must be obtained before sending a request to the blood bank, and the intravenous line must be set before the PC is issued from the blood bank. Staff at the issue counter does the final checks for details such as patient ID, unit no, blood group, and abnormal appearance or clumps suggestive of infection in the PC bag before issuing the unit.

Special requirements such as leukoreduction to reduce HLA alloimmunization or to minimize CMV transmission, irradiation to prevent transfusion-associated graft vs. host disease (TAGvHD) might be needed in specific patient groups. This special request is mentioned on the blood request forms.

Technique

The patient should have an appropriate IV cannula whose size ranges from 14G to 26G. In an adult, we normally use size 18G to 22G, while in the pediatric age group, it ranges from 25G to 26G. In rare cases where IV access is not available intraosseous route can also be used for transfusion.

Pretransfusion medication has been used in certain situations such as antihistamines in patients with a previous history of an allergic reaction during transfusion, occasionally meperidine or corticosteroid are occasionally ordered in patients with a history of severe rigors during transfusion.

The patient’s pretransfusion vitals are recorded by the transfusions, thereafter connecting the PC bag by aseptically spiking the blood transfusion set to the IV line. A standard blood transfusion set with an inline filter of 170 to 260 micron is used. A transfusion rate of 2 to 5 ml/min is used, thereby completing the transfusion in 1 to 2 hours. Slower flow rates are used in patients at risk of fluid overload. The patient is closely monitored during the transfusion with the vitals recorded every 15 minutes if a transfusion reaction is suspected at any point, the transfusion is stopped immediately with management protocol followed.

Complications

Platelet transfusion can be associated with complications. These complications can be immune-mediated such as febrile non-hemolytic transfusion reaction (FNHTR), allergic/anaphylaxis, TAGvHD, transfusion-related acute lung injury (TRALI), post-transfusion purpura, transfusion-related immunomodulation (TRIM), platelet refractoriness or non-immune mediated such as transfusion-associated circulatory overload (TACO), physical injury, sepsis, viral infection transmission, hypotensive reaction.

Febrile Non-Hemolytic Transfusion Reaction (FNHTR)

FNHTR is a relatively common complication with a frequency of 4% to 30%. It is characterized by the temperature rise of ≥1°C within the first 4hr of transfusion, which resolves within 48 hours, there can be associated with nausea, vomiting, dyspnoea, and hypotension.  Antibodies against HLA or leukocyte antigen in donor plasma are most commonly implicated. Antigen present on donor white cells binds to the antibody in the recipient, which leads to pyrogen and cytokine release such as TNF-alpha, IL1, and IL6. FNHTR can also occur due to biologic response modifiers (BRM) released during platelet storage, which is increased with storage. Platelet has maximum storage allowed for five days during which the release of substances such as CD40L, IL6, and IL8 can occur. FNHTR is diagnosed with the above-mentioned features and the possibility of chills, hemolytic causes are ruled out by further immunohematology workup and lab findings. FNHTR can be minimized by leukoreduction and by platelet additive solution (PAS), which replaces maximum plasma in stored platelets.

Allergic and Anaphylaxis

An allergic reaction is similar to FNHTR, and its frequency is between 0.09% and 21%. It manifests as pruritus, urticaria, or systematically as bronchoconstriction and seldom associated with fever. Pathogenesis is heterogeneous in origin ranging from proteins, antibodies, cytokines to BRM released during storage.

Anaphylaxis can occur when the patient is IgA deficient and has antibodies against it and receives IgA-containing platelets, and this occurs 1 in 50,000 transfusions. Diagnosis is made clinically, and it is an emergency.it can be prevented by giving washed platelets or platelets obtained from IgA deficient donors.

Allergic reactions can be minimized by depleting plasma in platelets.

Transfusion-associated Graft vs. Host Disease

This a rare but fatal complication characterized by fever and multiple systemic manifestations such as skin, gastrointestinal tract, liver, and others. It is caused by the transfusion of viable lymphocytes that get a favorable environment in the recipient, where they engraft and proliferate subsequently attacking the host tissues. It can occur between 1 to 6 weeks from transfusion and occurs in an immunocompromised host, those with congenital T-cell defects, a population with low genetic diversity (homozygous HLA), or first-degree patient relatives. Symptoms involve multiple organs as skin, the intestine, liver, and the suppression of bone marrow. Diagnosis is that of exclusion and requires molecular methods of testing apart from microscopic features seen. This can be prevented by the irradiation of platelets.

TRAIL

TRALI is another rare complication associated with the development of respiratory failure after ruling out other possible causes. Mainly caused by transfusion of antibodies in the plasma from the donor against HLA or human neutrophil antigens, an example is a platelet donated by a multiparous woman. TRALI occurs within 6 hours of transfusion. These patient develop acute worsening respiratory symptoms with characteristic features as hypoxemia: PaO/FIO ≤ 300 mm Hg with oxygen saturation <90%, all other causes of acute lung injury are ruled out before considering TRALI, it can be minimized by reducing plasma in platelets transfused such as the use of PAS.

Post Transfusion Purpura

A rare syndrome with a sudden drop in platelet count within 1 to 21 days of platelet transfusion, it is a self-limiting condition associated with wet purpura. Believed to be caused by autoantibody formation as a complication to platelet transfusion.

Transfusion-related Immunomodulation

The presence of leukocytes and biologic response modifiers released during storage have been implicated in immunomodulation. TRIM leads to a modified response of TH1/Th2 T-cells, which predisposed the patient to infection and delayed recovery from surgery. This can also be prevented by prestorage leukoreduction and depleting plasma from platelets. 

Platelet Refractoriness

This occurs when post-transfusion platelet recovery is not as expected. Though multiple causes can be there ranging from immune to non-immune, a multi transfused patient can develop antibodies against specific HPA(human platelet antigens) or HLA antigens. These antibodies are implicated in platelet refractoriness.  the antibodies cause platelet destruction by the immune system; in such patients, platelet crossmatching can reduce the incidence. HLA matched platelets, or if anti-human platelet antigen(HPA) antibody is involved matching HPA antigen is indicated.

Transfusion Associated Circulatory Overload

This adverse reaction is more likely in the pediatric group and patients with cardiac insufficiency. Slow transfusion with close monitoring in risk group is recommended

Physical Injury

This is possible at the site of intravenous access, which can cause complications like hematoma or nerve injury.

Sepsis and Bacterial Infection

Platelet concentrates are stored up to 5 days at temperatures 22 to 24 degrees C. This temperature is favorable for the growth of bacteria like Staphylococcus aureus and gram-negative bacteria. Possible sources of infections can be improper cleansing of donor phlebotomy site or if a donor has asymptomatic bacteremia. The risk of infection to the patient ranges from 0.14% to 1.41% with platelet transfusion. Pathogen reduction technology has been used to minimize infections in plasma and platelets.

Transmission of Viral Infection

All blood donations are screened for HIV, HCV, and HBV with other virus screening depending on the region. There remains a residual risk of transmission, as not all donors in the window period are detected. There is a possibility of transmission of infection by other viruses that are not routinely screened in the blood bank, more so of emerging infections. Pathogen reduction technology has been used to reduce this risk, but it’s not effective against all types of viruses.

Hypotensive Reaction

Patient on ACE inhibitors who receive bedside leukoreduction is at risk of hypotension. Exposure of the blood component to the negatively charged surface of the filter produces vasoactive bradykinin-related peptides, and this occurs within 5 minutes of transfusion. With ACE inhibitors present in the patient, these peptides are not metabolized, leading to hypotension. A proper history of medications before transfusion is important.

References

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Parathyroidectomy/ Thyroid Surgery – Indications, Contraindication

Parathyroidectomy is the surgery to remove one or more of the parathyroid glands in the patient who has hyperparathyroidism with a varies of etiology. This activity reviews the technique, complications of parathyroidectomy, and highlights the role of the interprofessional team in evaluating and managing the patients undergoing parathyroidectomy perioperatively.

Parathyroidectomy is the surgery to remove one or more of the parathyroid glands in the patient who has hyperparathyroidism with a varies of etiology. Parathyroidectomy is the only definitive treatment for primary hyperparathyroidism. The majority of patients with primary hyperparathyroidism have a single parathyroid adenoma. The traditional parathyroidectomy is to explore all four glands and remove the adenoma(s).

With the development of the preoperative localization technique, the minimally invasive surgery using the radio-guided technique, ultrasound imaging, high-resolution endoscopic technique, rapid intraoperative parathyroid hormone (IOPTH) monitoring has been used by many surgeons. The traditional parathyroidectomy still has its advantages and is the standard surgery that is reviewed in this article.

Anatomy and Physiology

The parathyroid glands are 4 glands located posterior to the thyroid, weighted 30-50 mg. The 2 superior parathyroid glands are derived from the fourth pharyngeal pouch, more constant located in the neck, posterior to the recurrent laryngeal nerve. The 2 inferior parathyroid glands are derived from the third pharyngeal pouch as well as thymus, they are mostly located inferior to the thyroid and anterior to the recurrent laryngeal nerve, but sometimes they can migrate to the lower neck or behind the sternum. The Ectopic glands may be located in the carotid sheath, paraesophageal or intrathyroidal position.

The 4 parathyroid glands are supplied by the inferior thyroid artery from the thyrocervical trunk. The superior parathyroid glands may be supplied by the superior thyroid artery or by an anastomotic branch between the inferior thyroid and the superior thyroid artery in 20% of cases.

Parathyroid glands regulate calcium by secreting Parathyroid Hormone (PTH). When the serum calcium level decreases, the chief cells in the parathyroid release PTH. In the kidney, PTH increases calcium re-absorption, excretion of phosphate, and promotes 25-hydroxy vitamin D converting to active 1,25-dihydroxy Vitamin D-3. In the bone, PTH stimulates osteoclast activity and releases calcium into the blood, and elevates serum calcium level. In the intestine, activated Vitamin D increases the absorption of calcium.

Hyperparathyroidism is a disorder with excessive production of PTH due to the overactivity of the parathyroid gland. Primary hyperparathyroidism is caused by autonomous hypersecretion of PTH from the abnormal parathyroid gland. The majority of patients with primary hyperparathyroidism have a single enlarged parathyroid gland, mostly adenoma. In rare cases, multiple endocrine neoplasia (MEN) type 1, type 2A, or parathyroid carcinoma can cause primary hyperparathyroidism. The high level of calcium due to hypersecretion of PTH can lead to neuromuscular symptoms, osteoporosis and bone loss, and kidney stones.

Secondary hyperparathyroidism is due to high PTH levels from the physiological response to hypocalcemia. Vitamin D deficiency and chronic renal failure are the most common causes of secondary hyperparathyroidism.

Tertiary hyperparathyroidism occurs in patients with secondary hyperparathyroidism from chronic renal failure and persistent secretion of PTH after renal transplant.

Indications

Primary Hyperparathyroidism

Parathyroidectomy is indicated for all patients with symptomatic primary hyperparathyroidism. The symptoms include polydipsia and polyuria, Nephrolithiasis or nephrocalcinosis, hypercalciuria (24-hour urine calcium level >400 mg/dL), Impaired renal function (glomerular filtration rate [GFR] <60 mL/minute), Osteoporosis (bone density score <-2.5), fragility fracture or vertebral compression fracture, pancreatitis, peptic ulcer disease or gastroesophageal reflux and neurocognitive dysfunction or neuropsychiatric symptoms attributable to PHPT.

Indications of Parathyroidectomy in Asymptomatic Hyperparathyroidism

Age younger than 50 years, Serum calcium level >1 mg/dL above the normal limit, Urinary calcium excretion > 400 mg per 24 hours (10 mmol per day), Creatinine clearance reduced by more than 30 percent compared with age-matched persons, Bone density (lumbar spine, hip, or forearm) that is > 2.5 standard deviations below peak bone mass (T score -2.5), Medical surveillance not desirable or possible, and Surgery requested by the patient.

A recent study revealed normocalcemic and hypercalcemic primary hyperparathyroidism had similarly increased cardiovascular risk factors. Parathyroidectomy ameliorated the increased cardiovascular risk factors in both normocalcemic and hypercalcemic PHPT.

Secondary Hyperparathyroidism

Patients with secondary hyperparathyroidism are usually managed medically. Parathyroidectomy is indicated in refractory hyperparathyroidism with hypercalcemia or hyperphosphatemia or severe symptoms. About 15% of patients will need parathyroidectomy for medically refractory secondary hyperparathyroidism after 5 to 10 years on dialysis.

Tertiary Hyperparathyroidism

Tertiary hyperparathyroidism with symptomatic hypercalcemia is the main indication for parathyroidectomy. Surgical treatment for tertiary HPT has higher cure rates than medical therapy. Limited or subtotal parathyroidectomy is recommended. The goal is a normal calcium level at least 6 months postoperatively.

Parathyroidectomy is indicated if the hyperparathyroidism is suspicion of parathyroid carcinoma, especially with significantly elevated calcium or PTH levels, painful large neck mass, or inhomogeneous mass on imaging.

Other indications of parathyroidectomy include parathyroid cyst, parathyroid hypercalcemic crisis (severe hypercalcemia and central nervous system dysfunction).

Contraindications

  • Absolute Contraindication – Parathyroidectomy is contraindicated in patients with familial hypocalciuric hypercalcemia (FHH) presenting with elevated calcium and PTH levels but low 24-hour urine calcium excretion and a low ratio of 24-hour urinary calcium to creatinine clearance.  Parathyroidectomy does not cure FHH -associated hypercalcemia.
  • Relative Contraindication – Contralateral recurrent laryngeal nerve (RLN) injury or vocal cord dysfunction.

Equipment

The following equipment is needed:

  • Bovie or bipolar cautery, harmonic scalpel, LigaSure, or surgical ties.
  • Frozen pathology analysis to confirm parathyroid tissue.
  • Intraoperative nerve monitoring (IONM): RLN monitoring is an attempt to reduce the risk of nerve injury during parathyroid surgery, especially in re-operative parathyroid surgery.
  • In focused parathyroidectomy, ultrasound or Gamma probe can be used to localize abnormal gland intraoperatively, Intraoperative parathyroid hormone (IOPTH) assay to confirm the removal of the hyperfunctioning gland.

Personnel

Standard operating room staff, one or two surgeons, and the anesthesiologist.

Preparation

Surgery Plan

Parathyroidectomy is the standard treatment for hyperparathyroidism. The goal is to remove the parathyroid gland or glands producing excess PTH. For patients with multi-gland disease, unsuccessful preoperative localization, the traditional surgical approach of bilateral parathyroid exploration of 4 glands is the standard procedure. Focused parathyroidectomy with a smaller incision and less dissection is used in patients with a well-localized solitary adenoma. Compared to bilateral parathyroid exploration, focused parathyroidectomy has similar clinical outcomes: including recurrence, persistence, and reoperation rates but significantly lower overall complication rates and shorter operative time.

Total parathyroidectomy and subtotal parathyroidectomy (a small remnant of gland left or auto-transplanted) are indicated in secondary or tertiary hyperparathyroidism with parathyroid hyperplasia. Total parathyroidectomy with auto-transplantation carries a higher risk of permanent hypocalcemia and cardiovascular events whereas the risk of hyperparathyroidism recurrence is higher with subtotal parathyroidectomy.  Several new technologies including ultrasound localization, of hyperplastic parathyroid glands, radio-guided surgery, endoscopic-assisted parathyroidectomy, and intraoperative assessment of serum PTH levels can be appropriately used in the practice of parathyroid surgery.

Preoperative Localization

Preoperative localization is critical for focused, minimally invasive parathyroid surgery. The localization imaging studies include Sestamibi scintigraphy (technetium-99-sestamibi scanning), SPECT — Sestamibi-single photon emission computed tomography (SPECT or MIBI-SPECT), SPECT and CT fusion, neck ultrasound, 4D-CT, MRI, and PET-CT. In the cases with a history of neck surgery, unsuccessful radio-image localization, invasive localization such as selective venous sampling.

Pre-op Preparation

Anesthesia

General anesthesia is preferred for parathyroidectomy, especially for patients who need sternotomy, neck dissection. Most surgeons prefer to use general anesthesia with intubation for single gland, focused parathyroidectomy. Recent studies showed local anesthesia with the cervical block is feasible, and significantly reduce the cost. Local anesthesia in minimally invasive parathyroidectomy was associated with significantly lower postoperative pain, nausea, and vomiting. General anesthesia is preferred for parathyroidectomy, especially for the patients who need sternotomy, neck dissection.

Position

The patient is placed on the operating table in a supine position with the neck extended and both arms tucked at the sides. A shoulder roll can be placed to improve the exposure of the neck. The operating table is slightly placed in reverse Trendelenburg position. Patients with cervical spine disease should be assessed for the safety of neck extension.

Technique

Procedure

  • In bilateral exploration, a 6 cm transverse low collar incision is made about one finger wide above the clavicular head in a skin crease. The dissection carries down to subcutaneous tissue and the platysma muscle. Hemostasis is obtained by electrocautery or ligation using silk.
  • Dissection continues to elevate the upper subplatysmal flap to the thyroid notch and the lower flap to the sternal notch. The self-retaining retractors are used to retract the skin flaps.
  • The deep fascia is opened by a midline incision along the raphe of the strap muscle. Dissect The fascia along the anterior margins of the sternocleidomastoid muscle, and divide the sternohyoid muscles and sternothyroid muscles vertically. Blunt dissect to the plane of cleavage between the sternocleidomastoid muscle and the outer boundaries of the sternothyroid muscle.
  • A midline vertical incision is made between the sternohyoid muscles, extending from the thyroid notch to the level of the sternal notch. The sternohyoid muscles are then elevated to develop a plane between the thyroid gland and the sternohyoid muscles. Blunt dissection with the index finger in the plane to the lateral edge of the thyroid freezes the entire lateral surface of the thyroid and exposes the space between the trachea and carotid sheath.
  • Ligate the middle thyroid vein, then retract the thyroid lobe medially and anteriorly, the recurrent laryngeal nerve and the parathyroid glands can be identified at the upper and lower poles of the thyroid lobe. A similar exploration is made on the other side.  The serum sample of PTH is collected for the baseline level.
  • The solitary adenoma appears to be enlarged in size and discolored. The enlarged gland is dissected and divided from the surrounding tissue without injuring the recurrent laryngeal nerve especially isolating the inferior parathyroid glands. It is important not to rupture the gland capsule in cases of malignancy but also in benign disease to prevent parathyromatosis.
  • The tissue specimen is sent for frozen section pathology to confirm it is the parathyroid gland. The PTH serum level is repeated, the removal of the overactive parathyroid gland is confirmed if the level drops >50%. Continue to explore additional adenoma if the PTH level doesn’t fall to the expected level.
  • Irrigate the wound, approximate the strap muscles with interrupted absorbable sutures, close the platysma with interrupted absorbable suture, close the skin with a running subcuticular absorbable suture.
  • With preoperative localization of abnormal parathyroid gland, focused parathyroidectomy can be performed only in the imaging identified area. The incision size, the extent of dissection, and the duration of surgery are limited.

Intraoperative Decision Making

  • It is important to fully mobilize the thyroid to search for a missing parathyroid gland. If the upper gland is missing, explore the tracheoesophageal groove, the retropharyngeal space, and above the thyroid cartilage.  The search for a missing lower gland should begin with a thorough exploration of the inferior pole of the thyroid and the surrounding soft tissue. If the gland is not found, performing a formal cervical thymectomy (or at least pulling up the thymus for examination is reasonable).
  • In the patient with 4 gland hyperplasia, remove 3 and a half glands. The remnant half gland can be left in situ or implanted into the sternocleidomastoid muscle. In some patients with secondary or tertiary hyperparathyroidism, total parathyroidectomy with subcutaneous forearm autotransplantation is recommended.
  • For patients with multiple endocrine neoplasia (MEN) type 1-associated PHPT, the initial surgical procedure usually includes resection of three-and-one-half hyperplastic parathyroid glands (subtotal resection) with strong consideration for concomitant cervical thymectomy. For patients with MEN type 2A-associated PHPT, parathyroid hyperplasia is heterogeneous, bilateral exploration is usually performed as the initial procedure, only the visibly enlarged glands are resected. For patients with MEN type 2A-associated recurrent hyperparathyroidism, a complete parathyroidectomy with forearm autotransplantation is typically performed.
  • Parathyroid carcinoma should be completely resected, requiring en bloc resection of the parathyroid mass, and any adjacent tissues have been invaded. Complete surgical resection with microscopically negative margins is the recommended treatment and offers the best chance of cure.

Complications

Postoperative Neck Bleeding and Hematoma – Postoperatively life-threatening hematoma is rare, the incidence reported was 0.6%. But it is a serious complication. The hematoma compresses the trachea, causes venous congestion of airway structures, and subsequent airway compromise.  Immediate wound opening and surgical hematoma evacuation or re-exploration are indicated to alleviate airway compression. Intubation should not be delayed.

Recurrent Laryngeal Nerve Injury – Recurrent laryngeal nerve injury is one of the most feared complications of parathyroid surgery. Injury to the recurrent laryngeal nerve results in paresis or palsy of the vocal cord causing hoarseness (unilateral damage) or stridor, airway occlusion (bilateral damage), and an increased risk of aspiration, may need immediate reintubation or occasionally tracheostomy. Most recurrent laryngeal nerve injuries are transient. 1.1% of the patient presented a permanent postoperative vocal cord paresis after thyroid and parathyroid surgery due to recurrent laryngeal nerve injury. Injuries after parathyroidectomy are less frequent compared to thyroid surgery. Most of the patients with transient postoperative recurrent laryngeal nerve injury recovered normal vocal cord mobility within 6 months. Identifying the recurrent laryngeal nerve during thyroid dissection is the gold standard to avoid nerve injury.

Intraoperative nerve monitoring during parathyroidectomy is a promising adjunct to visualization alone in detecting nerve structures during neck dissection, which may decrease the likelihood of recurrent laryngeal nerve injury. A reinnervation procedure should be attempted When recurrent laryngeal nerve transection is recognized during parathyroidectomy.

Hypoparathyroidism and Hypocalcemia – The symptoms of postoperative hypocalcemia include perioral numbness, fingertip paresthesia, Chvostek’s sign, Trousseau’s sign, and severe symptoms including tetany, cardiac dysrhythmia, seizures. Most hypocalcemia is transient, and permanent hypocalcemia is reported in only 0.5% to 3.8% of cases. One of the most common causes of postsurgical hypoparathyroidism and hypocalcemia is inadvertent removal of, damage to, or inadvertent devascularization of the parathyroid glands.  Postoperative hypocalcemia may be due to “Hungry bone syndrome” with low serum calcium levels resulting from remineralization of the bone as the stimulus of PTH for high bone turnover is removed after parathyroid surgery. As the American Association of Endocrine Surgeons Guidelines recommends, patients with transient postoperative hypoparathyroidism should be treated with calcium and, if necessary, calcitriol supplements, which should be weaned as tolerated. Patients with prolonged hypoparathyroidism may be considered for recombinant PTH therapy.

Persistent or Recurrent Hyperparathyroidism – Persistent/recurrent hyperparathyroidism occurs in 2% to 5% of patients with sporadic primary hyperparathyroidism. Persistent hyperparathyroidism should be defined as a failure to achieve normocalcemia within6months of parathyroidectomy. Recurrent hyperparathyroidism is defined by the recurrence of hypercalcemia after a normocalcemic interval at more than 6 months after parathyroidectomy.  The most common causes of persistent/recurrent hyperparathyroidism include unrecognized four gland hyperplasia, ectopic location of the hyperfunctioning parathyroid gland(s), or operations performed by inexperienced or low-volume parathyroid surgeons. A final intraoperative PTH level greater than 40 pg/mL was associated with an increased risk of persistent and recurrent disease irrespective of the number of glands resected.

The subsequent operation for persistent or recurrent hyperparathyroidism is often recommended to achieve a biochemical cure. But the indication is stricter than initial surgery due to lower cure rates and higher risks in the subsequent operation. Preop evaluation should be made by an experienced parathyroid surgeon, including confirmation of biochemical diagnosis, assessment of indications for surgery, review of prior records if available, and evaluation of RLN function.

Parathyroid Quick Facts

  • There are 4 parathyroids glands. We all have 4 parathyroids glands.
  • Except in rare cases, parathyroid glands are in the neck behind the thyroid.
  • Parathyroids are NOT related to the thyroid (except they are neighbors in the neck).
  • The thyroid gland controls much of your body’s metabolism, but the parathyroid glands control body calcium. They have no relationship except they are neighbors.
  • Parathyroid glands make a hormone, called “Parathyroid Hormone”.
  • Doctors and labs abbreviate Parathyroid Hormone as “PTH”.
  • Just like calcium, PTH has a normal range in our blood…we can measure it to see how good or bad a job the parathyroid glands are doing.
  • All four parathyroid glands do the exact same thing.
  • Parathyroid glands control the amount of calcium in your blood.
  • Parathyroid glands control the amount of calcium in your bones.
  • You can easily live with one (or even 1/2) parathyroid gland.
  • Removing all 4 parathyroid glands will cause very bad symptoms of too little calcium (hypoparathyroidism). HypOparathyroidism is the opposite of hypERparathyroidism and it is very rare… only one page of this entire site is about hypoparathyroidism disease.
  • When parathyroid glands go bad, it is just one gland that goes bad about 91% of the time–it just grows big (develops a benign tumor) and makes too much hormone. About 8% of the time people with hyperparathyroidism will have two bad glands. It is quite uncommon for 3 or 4 glands to go bad.
  • When one of your parathyroid glands goes bad and makes too much hormone, the excess hormone goes to the bones and takes calcium out of the bones, and puts it in your blood. It’s the high calcium in the blood that makes you feel bad.
  • Everybody with a bad parathyroid gland will eventually develop bad osteoporosis–unless the bad gland is removed.
  • Parathyroids almost never develop cancer–so stop worrying about that!
  • However, not removing the parathyroid tumor and leaving the calcium high for a number of years will increase the chance of developing other cancers in your body (breast, colon, kidney, and prostate).
  • There is only ONE way to treat parathyroid problems–Surgery.
  • Mini-Surgery is now available that almost everyone can/should have. You should educate yourself about the new surgical treatments available. Do not have an “exploratory” operation to find the bad parathyroid tumor–this old-fashioned operation is too big and dangerous.

References

 

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Vitamin B5 ; Symptoms, Food Source, Health Benefit

Vitamin B5 is a water-soluble vitamin ubiquitously found in plants and animal tissues with antioxidant properties. Vitamin B5 is a component of coenzyme A (CoA) and a part of the vitamin B2 complex. Vitamin B5 is a growth factor and is essential for various metabolic functions, including the metabolism of carbohydrates, proteins, and fatty acids. This vitamin is also involved in the synthesis of cholesterol, lipids, neurotransmitters, steroid hormones, and hemoglobin.

Vitamin B5  or Pantothenic acid is a water-soluble vitamin. Pantothenic acid is an essential nutrient. Animals require pantothenic acid in order to synthesize coenzyme-A (CoA), as well as to synthesize and metabolize proteins, carbohydrates, and fats. The anion is called pantothenate. Pantothenic acid is the amide between pantoic acid and β-alanine. Its name derives from the Greek pantothen, meaning from everywhere, and small quantities of pantothenic acid are found in nearly every food, with high amounts in fortified whole-grain cereals, egg yolks, liver, and dried mushrooms. It is commonly found as its alcohol analog, the provitamin panthenol (pantothenol), and calcium pantothenate.

Deficiency Symptoms of Vitamin B5

Pantothenic acid deficiency has only been observed in individuals who were fed diets virtually devoid of pantothenic acid or who were given a pantothenic acid metabolic antagonist, omega-methyl pantothenic acid. The subjects exhibited various degrees of signs and symptoms, including irritability and restlessness; fatigue; apathy; malaise; sleep disturbances; gastrointestinal complaints such as nausea, vomiting, and abdominal cramps; neurobiological symptoms such as numbness, paresthesias, muscle cramps, and staggering gait; and hypoglycemia and increased sensitivity to insulin.

Symptoms of a vitamin B5 deficiency may include

Recommended Intakes of Vitamin B5

Intake recommendations for pantothenic acid and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and sex, include:

  • Recommended Dietary Allowance (RDA) – Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals.
  • Adequate Intake (AI) – Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA.
  • Estimated Average Requirement (EAR) – Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals.
  • Tolerable Upper Intake Level (UL) – Maximum daily intake unlikely to cause adverse health effects.

When the FNB evaluated the available data, it found the data insufficient to derive an EAR for pantothenic acid. Consequently, the FNB established AIs for all ages based on usual pantothenic acid intakes in healthy populations.

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Adequate Intakes (AIs) for Pantothenic Acid 
Age Male Female Pregnancy Lactation
Birth to 6 months 1.7 mg 1.7 mg
7–12 months 1.8 mg 1.8 mg
1–3 years 2 mg 2 mg
4–8 years 3 mg 3 mg
9–13 years 4 mg 4 mg
14–18 years 5 mg 5 mg 6 mg 7 mg
19+ years 5 mg 5 mg 6 mg 7 mg

Dietary Reference Intakes for Pantothenic Acid by Life Stage Group (mg/day)

Adequate Intake
Life Stage Group
0-6 mo 1.7
7-12 mo 1.8
1-3 yr 2
4-8 yr 3
9-13 yr 4
14-18 yr 5
19-30 yr 5
31-50 yr 5
51-70 yr 5
> 70 yr 5
Pregnancy
< or = 18 yr 6
19-50 yr 6
Lactation
< or = 18 yr 7
19-50 yr 7

 

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Food Source of Vitamin B5

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Several food sources of pantothenic acid are listed bellow

 Selected Food Sources of Pantothenic Acid 
Food Milligrams
(mg) per
serving		 Percent
DV*
Breakfast cereals, fortified with 100% of the DV 10 100
Beef liver, boiled, 3 ounces 8.3 83
Shitake mushrooms, cooked, ½ cup pieces 2.6 26
Sunflower seeds, ¼ cup 2.4 24
Chicken, breast meat, skinless, roasted, 3 ounces 1.3 13
Tuna, fresh, bluefin, cooked, 3 ounces 1.2 12
Avocados, raw, ½ avocado 1.0 10
Milk, 2% milkfat, 1 cup 0.9 9
Mushrooms, white, stir-fried, ½ cup sliced 0.8 8
Potatoes, russet, flesh, and skin, baked, 1 medium 0.7 7
Egg, hard-boiled, 1 large 0.7 7
Greek yogurt, vanilla, nonfat, 5.3-ounce container 0.6 6
Ground beef, 85% lean meat, broiled, 3 ounces 0.6 6
Peanuts, roasted in oil, ¼ cup 0.5 5
Broccoli, boiled, ½ cup 0.5 5
Whole-wheat pita, 1 large 0.5 5
Chickpeas, canned, ½ cup 0.4 4
Rice, brown, medium-grain, cooked, ½ cup 0.4 4
Oats, regular and quick, cooked with water, ½ cup 0.4 4
Cheese, cheddar, 1.5 ounces 0.2 2
Carrots, chopped, raw, ½ cup 0.2 2
Cabbage, boiled, ½ cup 0.1 1
Clementine, raw, 1 clementine 0.1 1
Tomatoes, raw, chopped or sliced, ½ cup 0.1 1
Cherry tomatoes, raw, ½ cup 0 0
Apple, raw, slices, ½ cup 0 0

*DV = Daily Value. DVs were developed by the U.S. Food and Drug Administration (FDA) to help consumers compare the nutrient contents of products within the context of a total diet. The DV for the values in Table 2 is 10 mg for adults and children age 4 years and older. This value, however, decreases to 5 mg when the updated Nutrition and Supplement Facts labels are implemented. The updated labels must appear on food products and dietary supplements beginning in January 2020, but they can be used now. The FDA does not require food labels to list pantothenic acid content unless a food has been fortified with this nutrient. Foods providing 20% or more of the DV are considered to be high sources of a nutrient.

The U.S. Department of Agriculture’s (USDA’s) National Nutrient Database for Standard Reference website lists the nutrient content of many foods and provides a comprehensive list of foods containing pantothenic acid arranged by pantothenic acid content and by food name.

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Health Benefit of Pantothenic Acid / Vitamin B5

  • Pantothenic acid – has been used for a wide range of disorders such as acne, alopecia, allergies, burning feet, asthma, grey hair, dandruff, cholesterol-lowering, improving exercise performance, depression, osteoarthritis, rheumatoid arthritis, multiple sclerosis, stress, shingles, aging and Parkinson’s disease. It has been investigated in clinical trials for arthritis, cholesterol-lowering and exercise performance.[Mason P; Dietary Supplements,
  • The topical application of pantothenate –  is widely used in clinical practice for wound healing.
  • Pantothenic acid deficiency –  Taking pantothenic acid by mouth prevents and treats pantothenic acid deficiency.
  • Skin reactions from radiation therapy – Applying dexpanthenol, a chemical similar to pantothenic acid, to areas of irritated skin does not seem to help treat skin reactions from radiation therapy.
  • Some research suggests that taking pantothenic acid in combination with pantethine and thiamine does not improve muscular strength or endurance in well-trained athletes.
  • There is conflicting evidence regarding the usefulness of pantothenic acid in combination with large doses of other vitamins for the treatment of ADHD.
  • Early research suggests that taking dexpanthenol, a chemical similar to pantothenic acid, by mouth daily or receiving dexpanthenol shots can help treat constipation.
  • Early research suggests that using specific eye drops (Siccaprotect) containing dexpanthenol, a chemical similar to pantothenic acid, does not improve most symptoms of dry eyes.
  • Some evidence suggests that applying gel or drops containing dexpanthenol, a chemical similar to pantothenic acid, reduces some symptoms of eye trauma. However, not all research is consistent.
  • Early research suggests that pantothenic acid (given as calcium pantothenate) does not reduce symptoms of osteoarthritis.
  • There is inconsistent evidence on the potential benefits of taking pantothenic acid after surgery. Taking pantothenic acid or dexpanthenol, a chemical similar to pantothenic acid, does not seem to improve bowel function after stomach surgery. However, taking dexpanthenol by mouth might reduce other symptoms after surgery, such as sore throat.
  • Developing research suggests that pantothenic acid (given as calcium pantothenate) does not reduce the symptoms of arthritis in people with rheumatoid arthritis.
  • Early research suggests that using a specific spray (Nasicur) that contains dexpanthenol, a chemical similar to pantothenic acid, helps relieve nasal dryness.
  • Early research suggests that using a nasal spray containing dexpanthenol, a chemical similar to pantothenic acid, after sinus surgery reduces discharge from the nose, but not other symptoms.
  • Research on the effects of pantothenic acid for preventing skin irritations is not consistent. Some early research suggests that a specific product (Bepanthol Handbalsam) containing dexpanthenol, a chemical similar to pantothenic acid, does not prevent skin irritation when applied to the skin. However, other research suggests that dexpanthenol ointment can prevent skin irritation.
  • Early research suggests that using a specific ointment (Hepathrombin-50,000-Salbe Adenylchemie) containing dexpanthenol, a chemical similar to pantothenic acid, as well as heparin and allantoin reduces swelling related to ankle sprains.
  • Alcoholism.
  • Allergies.
  • Hair loss.
  • Asthma.
  • Heart problems.
  • Carpal tunnel syndrome.
  • Lung disorders.
  • Colitis.
  • Eye infections (conjunctivitis).
  • Convulsions.
  • Kidney disorders.
  • Dandruff.
  • Depression.
  • Diabetic problems.
  • Enhancing immune function.
  • Headache.
  • Hyperactivity.
  • Low blood pressure.
  • Inability to sleep (insomnia).
  • Irritability.
  • Multiple sclerosis.
  • Muscular dystrophy.
  • Muscle cramps.

References

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Esophageal Thrush Symptoms, Treatment, Prevention

Esophageal Thrush Symptoms/Esophageal candidiasis (EC) is one of the most common opportunistic infections in patients with impaired cellular immunity, and it is and the most common gastrointestinal (GI) opportunistic disorder among individuals infected with human immunodeficiency virus (HIV) ,  However, we have sometimes come across EC in healthy individuals without HIV infection.– When EC has been found in healthy individuals, predisposing medical conditions have often been identified.– Broad-spectrum antibiotics may eliminate certain bacteria that inhibit fungal growth, thereby enhancing Candida overgrowth. Soon after the introduction of H2-receptor antagonists, some isolated cases of digestive Candida were reported.

Causes of Esophageal Thrush

  • Invasive candidiasis – is caused by 15 of the more than 150 known species of Candida. These species, all confirmed by isolation from patients, are: C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, C. krusei, C. guilliermondii, C. lusitaniae, C. dubliniensis, C. pelliculosa, C. kefyr, C. lipolytica, C. famata, C. inconspicua, C. rugosa, and C. norvegensis. Over the last 20 – 30 years, C. albicans has been responsible for 95% of infections, with, C. glabrata, C. parapsilosis, C. tropicalis, and C. krusei causing the majority of the remaining cases.[rx]
  • Recently – C. auris, a species first reported in 2009, has been found to cause invasive candidiasis. C. auris has attracted attention because it can be resistant to the antifungal medications used to treat candidiasis.[rx]
  • Weakened immunity – Oral thrush is more likely to occur in infants and older adults due to reduced immunity. Some medical conditions and treatments can suppress your immune system, such as cancer and its treatments, organ transplantation and required drugs that suppress the immune system, and HIV/AIDS.
  • Diabetes – If you have untreated diabetes or the disease isn’t well-controlled, your saliva may contain large amounts of sugar, which encourages the growth of candida.
  • Vaginal yeast infections – Vaginal yeast infections are caused by the same fungus that causes oral thrush. You can pass the infection to your baby.
  • Medications. Drugs such as prednisone, inhaled corticosteroids, or antibiotics that disturb the natural balance of microorganisms in your body can increase your risk of oral thrush.
  • Other oral conditions – Wearing dentures, especially upper dentures, or having conditions that cause dry mouth can increase the risk of oral thrush.

Symptoms of Esophageal Thrush

The symptoms of esophageal thrush include

  • Some patients present with esophageal candidiasis as a first presentation of systemic candidiasis.
  • white lesions on the lining of your esophagus that may look like cottage cheese and may bleed if they’re scraped
  • People with esophageal candidiasis typically present with difficult or painful swallowing. Longstanding esophageal candidiasis can result in weight loss. There is often concomitant thrush in the mouth.
  • Pain or discomfort when swallowing
  • Dry mouth
  • Difficulty swallowing
  • Nausea
  • Vomiting
  • Weight loss
  • Chest pain
  • Creamy white patches on the inside of the cheeks and on surface of the tongue
  • White lesions on the roof of your mouth, tonsils, and gums
  • Cracking in the corner of your mouth
  • Especially red, sensitive, cracking, or itchy nipples
  • Stabbing pains felt deep within the breast
  • Significant pain when nursing or pain between nursing sessions

Diagnosis of Esophageal Thrush

These include

  • Endoscopic exam – In this procedure, your doctor examines your esophagus, stomach and upper part of your small intestine (duodenum) using a lighted, flexible tube with a camera on the tip (endoscope).
  • Physical exam – If needed, a physical exam and certain blood tests may be done to try to identify any possible underlying medical condition that could cause thrush in the esophagus.
  • Upper endoscopy – A test in which a long, flexible lighted tube, called an endoscope, is used to view the esophagus.
  • Biopsy – During this test, a small sample of the esophageal tissue is removed and then sent to a laboratory to be examined under a microscope.
  • Upper GI series (or barium swallow) – During this procedure, X-rays are taken of the esophagus after drinking a barium solution. Barium coats the lining of the esophagus and shows up white on an X-ray. This characteristic enables doctors to view certain abnormalities of the esophagus.

Treatment of Esophageal Candidiasis

The current first-line treatment is fluconazole, 200 mg. on the first day, followed by daily dosing of 100 mg. for at least 21 days total. Treatment should continue for 14 days after relief of symptoms. Other therapy options include:

  • Treatment of esophageal candidiasis involves the use of antifungal therapy. Unlike oropharyngeal candidiasis, esophageal candidiasis should always have therapy with systemic agents and not topical agents.
  • The most commonly used medication to treat esophageal candidiasis is oral fluconazole 200 to 400 mg per day for 14 to 21 days.
  • If patients cannot tolerate oral intake, then intravenous Fluconazole 400 mg daily can be used and then deescalated to oral Fluconazole when the patient can tolerate oral medications. Fluconazole 100 to 200 mg three times per week can be used to suppress recurrent esophageal candidiasis. Micafungin 150 mg IV daily has been shown to be non-inferior to fluconazole at 200 mg daily.
  • Itraconazole 200 mg per day orally or Voriconazole 200 mg twice daily for 14 to 21 days are other treatment options.
  • Amphotericin B deoxycholate 0.3 to 0.7 mg/kg daily can be used in patients with refractory candida esophagitis, but it has serious medication side effects and should be avoided if possible. Posaconazole 400 mg twice daily has been effective in refractory esophageal candidiasis as well. 
  • Since esophageal candidiasis is an opportunistic infection and most often seen in immunocompromised persons, the cause of the immunosuppression should be diagnosed and treated as well.
  • nystatin is not an effective treatment for esophageal candidiasis. It can be used as (swish, do not swallow) treatment for oral candidiasis that occurs with the use of asthma pumps.
  • other oral triazoles, such as itraconazole
  • caspofungin, used in refractory or systemic cases
  • amphotericin, used in refractory or systemic cases

Antifungals for oropharyngeal candidiasis

Antifungal agent Form Strength Usage Cost
Topical
Nystatin Pastille 200 000 units 1–2 pastilles, 4 times daily +
Suspension 5 mL swish-and-Swallow, 4 times daily +
+
Clotrimazole Oral troche 10 mg troche Dissolve 1 troche, 5 times daily +
Amphotericin B Suspension 1 mg/mL 1 mL swish-and-swallow, 4 times daily +
Lozenge 100 mg Four times daily +
Tablet 10 mg Four times daily +
Miconazole (Lauriad®) Lauriad 10 mg Apply to gum once daily TBD
Systemic
Ketoconazole Tablet 200 mg 1–2 tablets, once to twice daily +
Fluconazole Tablet 100 mg 1 tablet daily ++
Solution 10 mg/mL 10 mL, once daily ++
Itraconazole Capsule 100 mg 2 capsules, once daily ++
Solution 10 mg/mL 10–20 mL, once daily ++
Posaconazole Suspension 100 mg/2.5 mL 2 tsp daily +++
*Notes: Oral therapy preferred when tolerated. Cost index: (+) inexpensive; (++) modest expense; (+++) expensive; TBD = to be determined.

Antifungals for esophageal candidiasis

Antifungal agent Form Strength Usage
Azoles
Ketoconazole Tablets 200 mg 1–2 tablets, once to twice daily
Fluconazole Tablet 100 mg 1 tablet daily
SolutionIV piggyback 10 mg/mL 10 mL, once daily
100 mg, once daily
Itraconazole Capsule 100 mg 2 capsules, once daily
Solution 10 mg/mL 20 mL, once daily
Posaconazole Suspension 100 mg/2.5 mL 4 tsp, twice daily
Voriconazole Tablet/IV piggyback 200 mg Once daily
Caspofungin Intravenous 50 mg Once daily
Micafungin Intravenous 150 mg Once daily
Anidulafungin Intravenous 50 mg Once daily
Amphotericin B Intravenous 0.3–0.7 mg/kg Once daily

Treatment for Recommendations

  • An echinocandin (caspofungin: loading dose 70 mg, then 50 mg daily; micafungin: 100 mg daily; anidulafungin: loading dose 200 mg, then 100 mg daily) is recommended as initial therapy (strong recommendation; high-quality evidence).
  • Fluconazole, intravenous or oral, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily is an acceptable alternative to an echinocandin as initial therapy in selected patients, including those who are not critically ill and who are considered unlikely to have a fluconazole-resistant Candida species (strong recommendation; high-quality evidence).
  • Testing for azole susceptibility is recommended for all bloodstream and other clinically relevant Candida isolates. Testing for echinocandin susceptibility should be considered in patients who have had prior treatment with an echinocandin and among those who have infection with C. glabrata or C. parapsilosis (strong recommendation; low-quality evidence).
  • Transition from an echinocandin to fluconazole (usually within 5–7 days) is recommended for patients who are clinically stable, have isolates that are susceptible to fluconazole (eg, C. albicans), and have negative repeat blood cultures following initiation of antifungal therapy (strong recommendation; moderate-quality evidence).
  • For infection due to C. glabrata, transition to higher-dose fluconazole 800 mg (12 mg/kg) daily or voriconazole 200–300 (3–4 mg/kg) twice daily should only be considered among patients with fluconazole-susceptible or voriconazole-susceptible isolates (strong recommendation; low-quality evidence).
  • Lipid formulation amphotericin B (AmB) (3–5 mg/kg daily) is a reasonable alternative if there is intolerance, limited availability, or resistance to other antifungal agents (strong recommendation; high-quality evidence).
  • Transition from AmB to fluconazole is recommended after 5–7 days among patients who have isolates that are susceptible to fluconazole, who are clinically stable, and in whom repeat cultures on antifungal therapy are negative (strong recommendation; high-quality evidence).
  • Among patients with suspected azole- and echinocandin-resistant Candidainfections, lipid formulation AmB (3–5 mg/kg daily) is recommended (strong recommendation; low-quality evidence).
  • Voriconazole 400 mg (6 mg/kg) twice daily for 2 doses, then 200 mg (3 mg/kg) twice daily is effective for candidemia, but offers little advantage over fluconazole as initial therapy (strong recommendation; moderate-quality evidence).Voriconazole is recommended as step-down oral therapy for selected cases of candidemia due to C. krusei (strong recommendation; low-quality evidence).
  • All nonneutropenic patients with candidemia should have a dilated ophthalmological examination, preferably performed by an ophthalmologist, within the first week after diagnosis (strong recommendation; low-quality evidence).
  • Follow-up blood cultures should be performed every day or every other day to establish the time point at which candidemia has been cleared (strong recommendation; low-quality evidence).
  • Recommended duration of therapy for candidemia without obvious metastatic complications is for 2 weeks after documented clearance of Candida species from the bloodstream and resolution of symptoms attributable to candidemia (strong recommendation; moderate-quality evidence).

II. Should Central Venous Catheters Be Removed in Nonneutropenic Patients With Candidemia?

Recommendation

  • Central venous catheters (CVCs) should be removed as early as possible in the course of candidemia when the source is presumed to be the CVC and the catheter can be removed safely; this decision should be individualized for each patient (strong recommendation; moderate-quality evidence).

III. What Is the Treatment for Candidemia in Neutropenic Patients?

Recommendations

  • An echinocandin (caspofungin: loading dose 70 mg, then 50 mg daily; micafungin: 100 mg daily; anidulafungin: loading dose 200 mg, then 100 mg daily) is recommended as initial therapy (strong recommendation; moderate-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, is an effective but less attractive alternative because of the potential for toxicity (strong recommendation; moderate-quality evidence).
  • Fluconazole, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily, is an alternative for patients who are not critically ill and have had no prior azole exposure (weak recommendation; low-quality evidence).
  • Fluconazole, 400 mg (6 mg/kg) daily, can be used for step-down therapy during persistent neutropenia in clinically stable patients who have susceptible isolates and documented bloodstream clearance (weak recommendation; low-quality evidence).
  • Voriconazole, 400 mg (6 mg/kg) twice daily for 2 doses, then 200–300 mg (3–4 mg/kg) twice daily, can be used in situations in which additional mold coverage is desired (weak recommendation; low-quality evidence). Voriconazole can also be used as step-down therapy during neutropenia in clinically stable patients who have had documented bloodstream clearance and isolates that are susceptible to voriconazole (weak recommendation; low-quality evidence).
  • For infections due to C. krusei, an echinocandin, lipid formulation AmB, or voriconazole is recommended (strong recommendation; low-quality evidence).
  • Recommended minimum duration of therapy for candidemia without metastatic complications is 2 weeks after documented clearance of Candida from the bloodstream, provided neutropenia and symptoms attributable to candidemia have resolved (strong recommendation; low-quality evidence).
  • Ophthalmological findings of choroidal and vitreal infection are minimal until recovery from neutropenia; therefore, dilated funduscopic examinations should be performed within the first week after recovery from neutropenia (strong recommendation; low-quality evidence).
  • In the neutropenic patient, sources of candidiasis other than a CVC (eg, gastrointestinal tract) predominate. Catheter removal should be considered on an individual basis (strong recommendation; low-quality evidence).
  • Granulocyte colony – stimulating factor (G-CSF)–mobilized granulocyte transfusions can be considered in cases of persistent candidemia with anticipated protracted neutropenia (weak recommendation; low-quality evidence).

IV. What Is the Treatment for Chronic Disseminated (Hepatosplenic) Candidiasis?

Recommendations

  • Initial therapy with lipid formulation AmB, 3–5 mg/kg daily OR an echinocandin (micafungin: 100 mg daily; caspofungin: 70-mg loading dose, then 50 mg daily; or anidulafungin: 200-mg loading dose, then 100 mg daily), for several weeks is recommended, followed by oral fluconazole, 400 mg (6 mg/kg) daily, for patients who are unlikely to have a fluconazole-resistant isolate (strong recommendation; low-quality evidence).
  • Therapy should continue until lesions resolve on repeat imaging, which is usually several months. Premature discontinuation of antifungal therapy can lead to relapse (strong recommendation; low-quality evidence).
  • If chemotherapy or hematopoietic cell transplantation is required, it should not be delayed because of the presence of chronic disseminated candidiasis, and antifungal therapy should be continued throughout the period of high risk to prevent relapse (strong recommendation; low-quality evidence).
  • For patients who have debilitating persistent fevers, short-term (1–2 weeks) treatment with nonsteroidal anti-inflammatory drugs or corticosteroids can be considered (weak recommendation; low-quality evidence).

V. What Is the Role of Empiric Treatment for Suspected Invasive Candidiasis in Nonneutropenic Patients in the Intensive Care Unit?

Recommendations

  • Empiric antifungal therapy should be considered in critically ill patients with risk factors for invasive candidiasis and no other known cause of fever and should be based on clinical assessment of risk factors, surrogate markers for invasive candidiasis, and/or culture data from nonsterile sites (strong recommendation; moderate-quality evidence). Empiric antifungal therapy should be started as soon as possible in patients who have the above risk factors and who have clinical signs of septic shock (strong recommendation; moderate-quality evidence).
  • Preferred empiric therapy for suspected candidiasis in nonneutropenic patients in the intensive care unit (ICU) is an echinocandin (caspofungin: loading dose of 70 mg, then 50 mg daily; micafungin: 100 mg daily; anidulafungin: loading dose of 200 mg, then 100 mg daily) (strong recommendation; moderate-quality evidence).
  • Fluconazole, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily, is an acceptable alternative for patients who have had no recent azole exposure and are not colonized with azole-resistant Candida species (strong recommendation; moderate-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, is an alternative if there is intolerance to other antifungal agents (strong recommendation; low-quality evidence).
  • Recommended duration of empiric therapy for suspected invasive candidiasis in those patients who improve is 2 weeks, the same as for treatment of documented candidemia (weak recommendation; low-quality evidence).
  • For patients who have no clinical response to empiric antifungal therapy at 4–5 days and who do not have subsequent evidence of invasive candidiasis after the start of empiric therapy or have a negative non-culture-based diagnostic assay with a high negative predictive value, consideration should be given to stopping antifungal therapy (strong recommendation; low-quality evidence).

VI. Should Prophylaxis Be Used to Prevent Invasive Candidiasis in the Intensive Care Unit Setting?

Recommendations

  • Fluconazole, 800-mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) daily, could be used in high-risk patients in adult ICUs with a high rate (>5%) of invasive candidiasis (weak recommendation; moderate-quality evidence).
  • An alternative is to give an echinocandin (caspofungin: 70-mg loading dose, then 50 mg daily; anidulafungin: 200-mg loading dose and then 100 mg daily; or micafungin: 100 mg daily) (weak recommendation; low-quality evidence).
  • Daily bathing of ICU patients with chlorhexidine, which has been shown to decrease the incidence of bloodstream infections including candidemia, could be considered (weak recommendation; moderate-quality evidence).

VII. What Is the Treatment for Neonatal Candidiasis, Including Central Nervous System Infection?

What Is the Treatment for Invasive Candidiasis and Candidemia?

Recommendations

  • AmB deoxycholate, 1 mg/kg daily, is recommended for neonates with disseminated candidiasis (strong recommendation; moderate-quality evidence).
  • Fluconazole, 12 mg/kg intravenous or oral daily, is a reasonable alternative in patients who have not been on fluconazole prophylaxis (strong recommendation; moderate-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, is an alternative, but should be used with caution, particularly in the presence of urinary tract involvement (weak recommendation; low-quality evidence).
  • Echinocandins should be used with caution and generally limited to salvage therapy or to situations in which resistance or toxicity preclude the use of AmB deoxycholate or fluconazole (weak recommendation; low-quality evidence).
  • A lumbar puncture and a dilated retinal examination are recommended in neonates with cultures positive for Candida species from blood and/or urine (strong recommendation; low-quality evidence).
  • Computed tomographic or ultrasound imaging of the genitourinary tract, liver, and spleen should be performed if blood cultures are persistently positive for Candida species (strong recommendation; low-quality evidence).
  • CVC removal is strongly recommended (strong recommendation; moderate-quality evidence).
  • The recommended duration of therapy for candidemia without obvious metastatic complications is for 2 weeks after documented clearance of Candidaspecies from the bloodstream and resolution of signs attributable to candidemia (strong recommendation; low-quality evidence).

What Is the Treatment for Central Nervous System Infections in Neonates?

Recommendations

  • For initial treatment, AmB deoxycholate, 1 mg/kg intravenous daily, is recommended (strong recommendation; low-quality evidence).
  • An alternative regimen is liposomal AmB, 5 mg/kg daily (strong recommendation; low-quality evidence).
  • The addition of flucytosine, 25 mg/kg 4 times daily, may be considered as salvage therapy in patients who have not had a clinical response to initial AmB therapy, but adverse effects are frequent (weak recommendation; low-quality evidence).
  • For step-down treatment after the patient has responded to initial treatment, fluconazole, 12 mg/kg daily, is recommended for isolates that are susceptible to fluconazole (strong recommendation; low-quality evidence).
  • Therapy should continue until all signs, symptoms, and cerebrospinal fluid (CSF) and radiological abnormalities, if present, have resolved (strong recommendation; low-quality evidence).
  • Infected central nervous system (CNS) devices, including ventriculostomy drains and shunts, should be removed if at all possible (strong recommendation; low-quality evidence).

What Are the Recommendations for Prophylaxis in the Neonatal Intensive Care Unit Setting?

Recommendations

  • In nurseries with high rates (>10%) of invasive candidiasis, intravenous or oral fluconazole prophylaxis, 3–6 mg/kg twice weekly for 6 weeks, in neonates with birth weights <1000 g is recommended (strong recommendation; high-quality evidence)
  • Oral nystatin, 100 000 units 3 times daily for 6 weeks, is an alternative to fluconazole in neonates with birth weights <1500 g in situations in which availability or resistance preclude the use of fluconazole (weak recommendation; moderate-quality evidence).
  • Oral bovine lactoferrin (100 mg/day) may be effective in neonates <1500 g but is not currently available in US hospitals (weak recommendation; moderate-quality evidence).

VIII. What Is the Treatment for Intra-abdominal Candidiasis?

Recommendations

  • Empiric antifungal therapy should be considered for patients with clinical evidence of intra-abdominal infection and significant risk factors for candidiasis, including recent abdominal surgery, anastomotic leaks, or necrotizing pancreatitis (strong recommendation; moderate-quality evidence).
  • Treatment of intra-abdominal candidiasis should include source control, with appropriate drainage and/or debridement (strong recommendation; moderate-quality evidence).
  • The choice of antifungal therapy is the same as for the treatment of candidemia or empiric therapy for nonneutropenic patients in the ICU (See sections I and V) (strong recommendation; moderate-quality evidence).
  • The duration of therapy should be determined by adequacy of source control and clinical response (strong recommendation; low-quality evidence).

IX. Does the Isolation of Candida Species From the Respiratory Tract Require Antifungal Therapy?

Recommendation

  • Growth of Candida from respiratory secretions usually indicates colonization and rarely requires treatment with antifungal therapy (strong recommendation; moderate-quality evidence).

X. What Is the Treatment for Candida Intravascular Infections, Including Endocarditis and Infections of Implantable Cardiac Devices?

What Is the Treatment for Candida Endocarditis?

Recommendations

  • For native valve endocarditis, lipid formulation AmB, 3–5 mg/kg daily, with or without flucytosine, 25 mg/kg 4 times daily, OR high-dose echinocandin (caspofungin 150 mg daily, micafungin 150 mg daily, or anidulafungin 200 mg daily) is recommended for initial therapy (strong recommendation; low-quality evidence).
  • Step-down therapy to fluconazole, 400–800 mg (6–12 mg/kg) daily, is recommended for patients who have susceptible Candida isolates, have demonstrated clinical stability, and have cleared Candida from the bloodstream (strong recommendation; low-quality evidence).
  • Oral voriconazole, 200–300 mg (3–4 mg/kg) twice daily, or posaconazole tablets, 300 mg daily, can be used as step-down therapy for isolates that are susceptible to those agents but not susceptible to fluconazole (weak recommendation; very low-quality evidence).
  • Valve replacement is recommended; treatment should continue for at least 6 weeks after surgery and for a longer duration in patients with perivalvular abscesses and other complications (strong recommendation; low-quality evidence).
  • For patients who cannot undergo valve replacement, long-term suppression with fluconazole, 400–800 mg (6–12 mg/kg) daily, if the isolate is susceptible, is recommended (strong recommendation; low-quality evidence).
  • For prosthetic valve endocarditis, the same antifungal regimens suggested for native valve endocarditis are recommended (strong recommendation; low-quality evidence). Chronic suppressive antifungal therapy with fluconazole, 400–800 mg (6–12 mg/kg) daily, is recommended to prevent recurrence (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Infection of Implantable Cardiac Devices?

Recommendations

  • For pacemaker and implantable cardiac defibrillator infections, the entire device should be removed (strong recommendation; moderate-quality evidence).
  •  Antifungal therapy is the same as that recommended for native valve endocarditis (strong recommendation; low-quality evidence).
  • For infections limited to generator pockets, 4 weeks of antifungal therapy after removal of the device is recommended (strong recommendation; low-quality evidence).
  • For infections involving the wires, at least 6 weeks of antifungal therapy after wire removal is recommended (strong recommendation; low-quality evidence).
  • For ventricular assist devices that cannot be removed, the antifungal regimen is the same as that recommended for native valve endocarditis (strong recommendation; low-quality evidence). Chronic suppressive therapy with fluconazole if the isolate is susceptible, for as long as the device remains in place is recommended (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Suppurative Thrombophlebitis?

Recommendations

  • Catheter removal and incision and drainage or resection of the vein, if feasible, is recommended (strong recommendation; low-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, OR fluconazole, 400–800 mg (6–12 mg/kg) daily, OR an echinocandin (caspofungin 150 mg daily, micafungin 150 mg daily, or anidulafungin 200 mg daily) for at least 2 weeks after candidemia (if present) has cleared is recommended (strong recommendation; low-quality evidence).
  • Step-down therapy to fluconazole, 400–800 mg (6–12 mg/kg) daily, should be considered for patients who have initially responded to AmB or an echinocandin, are clinically stable, and have a fluconazole-susceptible isolate (strong recommendation; low-quality evidence).
  • Resolution of the thrombus can be used as evidence to discontinue antifungal therapy if clinical and culture data are supportive (strong recommendation; low-quality evidence).

XI. What Is the Treatment for Candida Osteoarticular Infections?

What Is the Treatment for Candida Osteomyelitis?

Recommendations

  • Fluconazole, 400 mg (6 mg/kg) daily, for 6–12 months OR an echinocandin (caspofungin 50–70 mg daily, micafungin 100 mg daily, or anidulafungin 100 mg daily) for at least 2 weeks followed by fluconazole, 400 mg (6 mg/kg) daily, for 6–12 months is recommended (strong recommendation; low-quality evidence).
  • Lipid formulation AmB, 3–5 mg/kg daily, for at least 2 weeks followed by fluconazole, 400 mg (6 mg/kg) daily, for 6–12 months is a less attractive alternative (weak recommendation; low-quality evidence).
  • Surgical debridement is recommended in selected cases (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Septic Arthritis?

  • Fluconazole, 400 mg (6 mg/kg) daily, for 6 weeks OR an echinocandin (caspofungin 50–70 mg daily, micafungin 100 mg daily, or anidulafungin 100 mg daily) for 2 weeks followed by fluconazole, 400 mg (6 mg/kg) daily, for at least 4 weeks is recommended (strong recommendation; low-quality evidence)
  • Lipid formulation AmB, 3–5 mg/kg daily, for 2 weeks, followed by fluconazole, 400 mg (6 mg/kg) daily, for at least 4 weeks is a less attractive alternative (weak recommendation; low-quality evidence).
  • Surgical drainage is indicated in all cases of septic arthritis (strong recommendation; moderate-quality evidence).
  • For septic arthritis involving a prosthetic device, device removal is recommended (strong recommendation; moderate-quality evidence).
  • If the prosthetic device cannot be removed, chronic suppression with fluconazole, 400 mg (6 mg/kg) daily, if the isolate is susceptible, is recommended (strong recommendation; low-quality evidence).

XII. What Is the Treatment for Candida Endophthalmitis?

What Is the General Approach to Candida Endophthalmitis?

Recommendations

  • All patients with candidemia should have a dilated retinal examination, preferably performed by an ophthalmologist, within the first week of therapy in nonneutropenic patients to establish if endophthalmitis is present (strong recommendation; low-quality evidence). For neutropenic patients, it is recommended to delay the examination until neutrophil recovery (strong recommendation; low-quality evidence).
  • The extent of ocular infection (chorioretinitis with or without macular involvement and with or without vitritis) should be determined by an ophthalmologist (strong recommendation; low-quality evidence).
  • Decisions regarding antifungal treatment and surgical intervention should be made jointly by an ophthalmologist and an infectious diseases physician (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Chorioretinitis Without Vitritis?

Recommendations

  • For fluconazole-/voriconazole-susceptible isolates, fluconazole, loading dose, 800 mg (12 mg/kg), then 400–800 mg (6–12 mg/kg) daily OR voriconazole, loading dose 400 mg (6 mg/kg) intravenous twice daily for 2 doses, then 300 mg (4 mg/kg) intravenous or oral twice daily is recommended (strong recommendation; low-quality evidence).
  • For fluconazole-/voriconazole-resistant isolates, liposomal AmB, 3–5 mg/kg intravenous daily, with or without oral flucytosine, 25 mg/kg 4 times daily is recommended (strong recommendation; low-quality evidence).
  • With macular involvement, antifungal agents as noted above PLUS intravitreal injection of either AmB deoxycholate, 5–10 µg/0.1 mL sterile water, or voriconazole, 100 µg/0.1 mL sterile water or normal saline, to ensure a prompt high level of antifungal activity is recommended (strong recommendation; low-quality evidence).
  • The duration of treatment should be at least 4–6 weeks, with the final duration depending on resolution of the lesions as determined by repeated ophthalmological examinations (strong recommendation; low-quality evidence).

What Is the Treatment for Candida Chorioretinitis With Vitritis?

Recommendations

  • Antifungal therapy as detailed above for chorioretinitis without vitritis, PLUS intravitreal injection of either amphotericin B deoxycholate, 5–10 µg/0.1 mL sterile water, or voriconazole, 100 µg/0.1 mL sterile water or normal saline is recommended (strong recommendation; low-quality evidence).
  • Vitrectomy should be considered to decrease the burden of organisms and to allow the removal of fungal abscesses that are inaccessible to systemic antifungal agents (strong recommendation; low-quality evidence).
  • The duration of treatment should be at least 4–6 weeks, with the final duration dependent on resolution of the lesions as determined by repeated ophthalmological examinations (strong recommendation; low-quality evidence).

XIII. What Is the Treatment for Central Nervous System Candidiasis?

Recommendations

  • For initial treatment, liposomal AmB, 5 mg/kg daily, with or without oral flucytosine, 25 mg/kg 4 times daily is recommended (strong recommendation; low-quality evidence).
  • For step-down therapy after the patient has responded to initial treatment, fluconazole, 400–800 mg (6–12 mg/kg) daily, is recommended (strong recommendation; low-quality evidence).
  • Therapy should continue until all signs and symptoms and CSF and radiological abnormalities have resolved (strong recommendation; low-quality evidence).
  • Infected CNS devices, including ventriculostomy drains, shunts, stimulators, prosthetic reconstructive devices, and biopolymer wafers that deliver chemotherapy should be removed if possible (strong recommendation; low-quality evidence).
  • For patients in whom a ventricular device cannot be removed, AmB deoxycholate could be administered through the device into the ventricle at a dosage ranging from 0.01 mg to 0.5 mg in 2 mL 5% dextrose in water (weak recommendation; low-quality evidence).

XIV. What Is the Treatment for Urinary Tract Infections Due to Candida Species?

What Is the Treatment for Asymptomatic Candiduria?

Recommendations

  • Elimination of predisposing factors, such as indwelling bladder catheters, is recommended whenever feasible (strong recommendation; low-quality evidence).
  • Treatment with antifungal agents is NOT recommended unless the patient belongs to a group at high risk for dissemination; high-risk patients include neutropenic patients, very low-birth-weight infants (<1500 g), and patients who will undergo urologic manipulation (strong recommendation; low-quality evidence).
  • Neutropenic patients and very low–birth-weight infants should be treated as recommended for candidemia (see sections III and VII) (strong recommendation; low-quality evidence).
  • Patients undergoing urologic procedures should be treated with oral fluconazole, 400 mg (6 mg/kg) daily, OR AmB deoxycholate, 0.3–0.6 mg/kg daily, for several days before and after the procedure (strong recommendation; low-quality evidence).

What Is the Treatment for Symptomatic Candida Cystitis?

Recommendations

  • For fluconazole-susceptible organisms, oral fluconazole, 200 mg (3 mg/kg) daily for 2 weeks is recommended (strong recommendation; moderate-quality evidence).
  • For fluconazole-resistant C. glabrata, AmB deoxycholate, 0.3–0.6 mg/kg daily for 1–7 days OR oral flucytosine, 25 mg/kg 4 times daily for 7–10 days is recommended (strong recommendation; low-quality evidence).
  • For C. krusei, AmB deoxycholate, 0.3–0.6 mg/kg daily, for 1–7 days is recommended (strong recommendation; low-quality evidence).
  • Removal of an indwelling bladder catheter, if feasible, is strongly recommended (strong recommendation; low-quality evidence).
  • AmB deoxycholate bladder irrigation, 50 mg/L sterile water daily for 5 days, may be useful for treatment of cystitis due to fluconazole-resistant species, such as C. glabrata and C. krusei (weak recommendation; low-quality evidence).

What Is the Treatment for Symptomatic Ascending Candida Pyelonephritis?

Recommendations

  • For fluconazole-susceptible organisms, oral fluconazole, 200–400 mg (3–6 mg/kg) daily for 2 weeks is recommended (strong recommendation; low-quality evidence).
  • For fluconazole-resistant C. glabrata, AmB deoxycholate, 0.3–0.6 mg/kg daily for 1–7 days with or without oral flucytosine, 25 mg/kg 4 times daily, is recommended (strong recommendation; low-quality evidence).
  • For fluconazole-resistant C. glabrata, monotherapy with oral flucytosine, 25 mg/kg 4 times daily for 2 weeks, could be considered (weak recommendation; low-quality evidence)
  • For C. krusei, AmB deoxycholate, 0.3–0.6 mg/kg daily, for 1–7 days is recommended (strong recommendation; low-quality evidence).
  • Elimination of urinary tract obstruction is strongly recommended (strong recommendation; low-quality evidence).
  • For patients who have nephrostomy tubes or stents in place, consider removal or replacement, if feasible (weak recommendation; low-quality evidence).

What Is the Treatment for Candida Urinary Tract Infection Associated With Fungus Balls?

Recommendations

  • Surgical intervention is strongly recommended in adults (strong recommendation; low-quality evidence).
  • Antifungal treatment as noted above for cystitis or pyelonephritis is recommended (strong recommendation; low-quality evidence).
  • Irrigation through nephrostomy tubes, if present, with AmB deoxycholate, 25–50 mg in 200–500 mL sterile water, is recommended (strong recommendation; low-quality evidence).

XV. What Is the Treatment for Vulvovaginal Candidiasis?

Recommendations

  • For the treatment of uncomplicated Candida vulvovaginitis, topical antifungal agents, with no one agent superior to another, are recommended (strong recommendation; high-quality evidence).
  • Alternatively, for the treatment of uncomplicated Candida vulvovaginitis, a single 150-mg oral dose of fluconazole is recommended (strong recommendation; high-quality evidence).
  • For severe acute Candida vulvovaginitis, fluconazole, 150 mg, given every 72 hours for a total of 2 or 3 doses, is recommended (strong recommendation; high-quality evidence).
  • For C. glabrata vulvovaginitis that is unresponsive to oral azoles, topical intravaginal boric acid, administered in a gelatin capsule, 600 mg daily, for 14 days is an alternative (strong recommendation; low-quality evidence).
  • Another alternative agent for C. glabrata infection is nystatin intravaginal suppositories, 100 000 units daily for 14 days (strong recommendation; low-quality evidence).
  • A third option for C. glabrata infection is topical 17% flucytosine cream alone or in combination with 3% AmB cream administered daily for 14 days (weak recommendation; low-quality evidence).
  • For recurring vulvovaginal candidiasis, 10–14 days of induction therapy with a topical agent or oral fluconazole, followed by fluconazole, 150 mg weekly for 6 months, is recommended (strong recommendation; high-quality evidence).

XVI. What Is the Treatment for Oropharyngeal Candidiasis?

Recommendations

  • For mild disease, clotrimazole troches, 10 mg 5 times daily, OR miconazole mucoadhesive buccal 50-mg tablet applied to the mucosal surface over the canine fossa once daily for 7–14 days are recommended (strong recommendation; high-quality evidence).
  • Alternatives for mild disease include nystatin suspension (100 000 U/mL) 4–6 mL 4 times daily, OR 1–2 nystatin pastilles (200 000 U each) 4 times daily, for 7–14 days (strong recommendation; moderate-quality evidence).
  • For moderate to severe disease, oral fluconazole, 100–200 mg daily, for 7–14 days is recommended (strong recommendation; high-quality evidence).
  • For fluconazole-refractory disease, itraconazole solution, 200 mg once daily OR posaconazole suspension, 400 mg twice daily for 3 days then 400 mg daily, for up to 28 days are recommended (strong recommendation; moderate-quality evidence).
  • Alternatives for fluconazole-refractory disease include voriconazole, 200 mg twice daily, OR AmB deoxycholate oral suspension, 100 mg/mL 4 times daily (strong recommendation; moderate-quality evidence).
  • Intravenous echinocandin (caspofungin: 70-mg loading dose, then 50 mg daily; micafungin: 100 mg daily; or anidulafungin: 200-mg loading dose, then 100 mg daily) OR intravenous AmB deoxycholate, 0.3 mg/kg daily, are other alternatives for refractory disease (weak recommendation; moderate-quality evidence).
  • Chronic suppressive therapy is usually unnecessary. If required for patients who have recurrent infection, fluconazole, 100 mg 3 times weekly, is recommended (strong recommendation; high-quality evidence).
  • For HIV-infected patients, antiretroviral therapy is strongly recommended to reduce the incidence of recurrent infections (strong recommendation; high-quality evidence).
  • For denture-related candidiasis, disinfection of the denture, in addition to antifungal therapy is recommended (strong recommendation; moderate-quality evidence).

XVII. What Is the Treatment for Esophageal Candidiasis?

Recommendations

  • Systemic antifungal therapy is always required. A diagnostic trial of antifungal therapy is appropriate before performing an endoscopic examination (strong recommendation; high-quality evidence).
  • Oral fluconazole, 200–400 mg (3–6 mg/kg) daily, for 14–21 days is recommended (strong recommendation; high-quality evidence).
  • For patients who cannot tolerate oral therapy, intravenous fluconazole, 400 mg (6 mg/kg) daily, OR an echinocandin (micafungin, 150 mg daily, caspofungin, 70-mg loading dose, then 50 mg daily, or anidulafungin, 200 mg daily) is recommended (strong recommendation; high-quality evidence).
  • A less preferred alternative for those who cannot tolerate oral therapy is AmB deoxycholate, 0.3–0.7 mg/kg daily (strong recommendation; moderate-quality evidence).
  • Consider de-escalating to oral therapy with fluconazole 200–400 mg (3–6 mg/kg) daily once the patient is able to tolerate oral intake (strong recommendation; moderate-quality evidence).
  • For fluconazole-refractory disease, itraconazole solution, 200 mg daily, OR voriconazole, 200 mg (3 mg/kg) twice daily either intravenous or oral, for 14–21 days is recommended (strong recommendation; high-quality evidence).
  • Alternatives for fluconazole-refractory disease include an echinocandin (micafungin: 150 mg daily; caspofungin: 70-mg loading dose, then 50 mg daily; or anidulafungin: 200 mg daily) for 14–21 days, OR AmB deoxycholate, 0.3–0.7 mg/kg daily, for 21 days (strong recommendation; high-quality evidence)
  • Posaconazole suspension, 400 mg twice daily, or extended-release tablets, 300 mg once daily, could be considered for fluconazole-refractory disease (weak recommendation; low-quality evidence).
  • For patients who have recurrent esophagitis, chronic suppressive therapy with fluconazole, 100–200 mg 3 times weekly, is recommended (strong recommendation; high-quality evidence).
  • For HIV-infected patients, antiretroviral therapy is strongly recommended to reduce the incidence of recurrent infections (strong recommendation; high-quality evidence).

Risk Factors

Patients with the following conditions, treatments or situations are at increased risk for invasive candidiasis.[rx][rx][rx]

  • Critical illness
  • Long-term intensive care unit stay
  • Abdominal surgery (aggravated by anastomotic leakage or repeat laparotomies)
  • Immunosuppressive diseases
  • Acute necrotizing pancreatitis
  • Malignant hematologic disease
  • Solid-organ transplantation
  • Hematopoietic stem cell transplantation
  • Solid-organ tumors
  • Neonates (especially low birth weight and preterm infants)
  • Broad-spectrum antibiotic treatment
  • Central venous catheter
  • Internal prosthetic device
  • Total parenteral nutrition
  • Hemodialysis
  • Glucocorticoid use
  • Chemotherapy
  • Noninvasive Candida colonization (particularly if multifocal)

Transmission

Invasive candidiasis is a nosocomial infection with the majority of cases associated with hospital stays.[rx]

Prevention

These measures may help reduce your risk of developing candida infections

  • Rinse your mouth – If you need to use a corticosteroid inhaler, be sure to rinse your mouth with water or brush your teeth after taking your medication.
  • Brush your teeth at least twice a day and floss daily – or as often as your dentist recommends.
  • Check your dentures – Remove your dentures at night. Make sure dentures fit properly and don’t cause irritation. Clean your dentures daily. Ask your dentist for the best way to clean your type of dentures.
  • See your dentist regularly – especially if you have diabetes or wear dentures. Ask your dentist how often you need to be seen.
  • Watch what you eat – Try limiting the amount of sugar-containing foods you eat. These may encourage the growth of candida.
  • Maintain good blood sugar control if you have diabetes – Well-controlled blood sugar can reduce the amount of sugar in your saliva, discouraging the growth of candida.
  • Treat a vaginal yeast infection – as soon as possible.
  • Treat dry mouth – Ask your doctor about ways to avoid or treat your dry mouth.
  • Avoid douching
  • Do not use feminine deodorant or deodorant pads or tampons
  • Wear underwear made from cotton or other natural fibers
  • Wear loose fitting pants or skirts
  • Wash underwear at a high temperature
  • Avoid tight underwear and pantyhose
  • Eat a healthy, varied diet
  • Promptly change wet clothing, for example bathing suits
  • Avoid hot tubs and hot baths

Home Remedies

Some home remedies include

  • Gentian violet – This is a dye made from coal tar. A person can apply it directly by swabbing it over thrush in the mouth, but they should not swallow it.
  • Probiotic-rich foods – Foods that contain probiotics, such as yogurt or cottage cheese, may help the body recover. These foods contain healthful bacteria that may help prevent the growth of thrush.
  • Probiotic supplements – Similarly to probiotic-rich foods, these supplements can help the body maintain its healthy bacteria. This may prevent a future thrush infection.

References

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Vitamin B Complex; Types, Deficiency Symptoms, Food Source

Vitamin B Complex/B vitamins are a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, they are chemically distinct compounds which often coexist in the same foods. In general, dietary supplements containing all eight are referred to as a vitamin B complex. Individual B vitamin supplements are referred to by the specific number or name of each vitamin.  Individual B vitamin supplements are referred to by the specific number or name of each vitamin – B1 = thiamine, B2 = riboflavin, B3 = niacin, etc. Some are better known by name than number niacin, pantothenic acid, biotin, and folate.

The recommended daily amount of each Vitamin B Complex/B vitamins

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For women and men, the recommended daily intake (RDI) for B vitamins are as follows

Women Men
B1 (Thiamine) 1.1 mg 1.2 mg
B2 (Riboflavin) 1.1 mg 1.3 mg
B3 (Niacin) 14 mg 16 mg
B5 (Pantothenic acid) 5 mg (RDI not established; Adequate Intake, or AI, provided) 5 mg (AI)
B6 (Pyridoxine) 1.3 mg 1.3 mg
B7 (Biotin) 30 mcg (AI) 30 mcg (AI)
B9 (Folate) 400 mcg 400 mcg
B12 (Cobalamin) 2.4 mcg 2.4 mcg

Older adults and women who are pregnant require higher amounts of B vitamins. Your doctor can provide dosage information tailored to your individual needs.

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Types of Vitamin B Complex/B vitamins

Thiamine (Vitamin B1)

  • Thiamine is a coenzyme in the pentose phosphate pathway, which is a necessary step in the synthesis of fatty acids, steroids, nucleic acids and the aromatic amino acid precursors to a range of neurotransmitters and other bioactive compounds essential for brain function [].
  • Thiamine plays a neuro-modulatory role in the acetylcholine neurotransmitter system, distinct from its actions as a cofactor during metabolic processes [] and contributes to the structure and function of cellular membranes, including neurons and neuroglia [].

Riboflavin (Vitamin B2)

  • The two flavoprotein coenzymes derived from riboflavin, FMN and FAD are crucial rates limiting factors in most cellular enzymatic processes. As an example, they are crucial for the synthesis, conversion, and recycling of niacin, folate and vitamin B6, and for the synthesis of all heme proteins, including hemoglobin, nitric oxide synthases, P450 enzymes, and proteins involved in electron transfer and oxygen transport and storage [].
  • The flavoproteins are also co-factors in the metabolism of essential fatty acids in brain lipids [], the absorption and utilization of iron [], and the regulation of thyroid hormones [].
  • Dysregulation of any of these processes by riboflavin deficiency would be associated with its own broad negative consequences for brain function. Riboflavin derivatives also have direct antioxidant properties and increase endogenous antioxidant status as essential cofactors in the glutathione redox cycle [].

Niacin (Vitamin B3)

  • A vast array of processes and enzymes involved in every aspect of peripheral and brain cell function are dependent on niacin derived nucleotides such as nicotinamide adenine dinucleotide (NAD) and NAD phosphate (NADP). Beyond energy production, these include oxidative reactions, antioxidant protection, DNA metabolism and repair, cellular signaling events (via intracellular calcium), and the conversion of folate to its tetrahydrofolate derivative [].
  • Niacin also binds agonistically at two G protein receptors, the high-affinity Niacin receptor 1 (NIACR1), responsible for the skin flush associated with high intake of niacin, and the low-affinity NIACR2. Niacin receptors are distributed both peripherally in immune cells and adipose tissue, and throughout the brain. Currently established roles include modulation of inflammatory cascades [,] and anti-atherogenic lipolysis in adipose tissue [,].
  • NIACR1 receptor populations have been shown to be down-regulated in the anterior cingulate cortex of schizophrenia sufferers [] and upregulated in the substantia nigra of Parkinson’s disease sufferers, (a group that have low niacin levels generally) with levels correlating with poorer sleep architecture in this group []. A recent case study demonstrated that 250 mg niacin administration modulated peripheral immune cell NIACR1 expression and attenuated the disturbed sleep architecture associated with Parkinson’s disease [].

Pantothenic Acid (Vitamin B5)

  • This vitamin is a substrate for the synthesis of the ubiquitous coenzyme A (CoA). Beyond its role in oxidative metabolism, CoA contributes to the structure and function of brain cells via its involvement in the synthesis of cholesterol, amino acids, phospholipids, and fatty acids. Of particular relevance, pantothenic acid, via CoA, is also involved in the synthesis of multiple neurotransmitters and steroid hormones [].

Vitamin B6 (Pyridoxine, Pyridoxal, Pyridoxamine)

  • Beyond its role as a necessary cofactor in the folate cycle (see above and folate section below), the role of vitamin B6 in amino acid metabolism makes it a rate-limiting cofactor in the synthesis of neurotransmitters such as dopamine, serotonin, γ-aminobutyric acid (GABA), noradrenaline and the hormone melatonin.
  • The synthesis of these neurotransmitters is differentially sensitive to vitamin B6 levels, with even mild deficiency resulting in preferential down-regulation of GABA and serotonin synthesis, leading to the removal of inhibition of neural activity by GABA and disordered sleep, behavior, and cardiovascular function and a loss of hypothalamus-pituitary control of hormone excretion.
  • Vitamin B6 also has a direct effect on immune function and gene transcription/expression [] and plays a role in brain glucose regulation [].
  • More broadly, levels of pyridoxal-5′-phosphate are associated with increased functional indices and biomarkers of inflammation, and levels of pyridoxal-5′-phosphate are down-regulated as a function of more severe inflammation [,], potentially as a consequence of pyridoxal-5′-phosphate’s role either in the metabolism of tryptophan or in one-carbon metabolism []. This role is particularly pertinent as inflammatory processes contribute to the etiology of numerous pathological states including dementia and cognitive decline [].

Biotin (Vitamin B7)

  • The brain is particularly sensitive to the delivery and metabolism of glucose. Biotin plays a key role in glucose metabolism and hemostasis, including regulation of hepatic glucose uptake, gluconeogenesis (and lipogenesis), insulin receptor transcription and pancreatic β-cell function [].
  • Frank deficiency in biotin is rarely reported, although lower circulating levels of biotin have been reported in those suffering glucoregulatory dysfunction, for instance, Type II diabetes, alongside an inverse relationship between fasting plasma glucose and biotin levels [].

Folate (Vitamin B9) and Vitamin B12 (Cobalamin)

  • The functions of these two vitamins are inextricably linked due to their complementary roles in the “folate” and “methionine” cycles. Indeed, a deficiency in vitamin B12 results in a functional folate deficiency, as folate becomes trapped in the form of methyltetrahydrofolate [,].
  • An actual or functional folate deficiency, with an attendant reduction in purine/pyrimidine synthesis and genomic and non-genomic methylation reactions in brain tissue, leads to decreased DNA stability and repair and gene expression/transcription, which could hamper neuronal differentiation and repair, promote hippocampal atrophy, demyelination and compromise the integrity of membrane phospholipids impairing the propagation of action potentials [].
  • Folate related downregulation of the synthesis of proteins and the nucleotides required for DNA/RNA synthesis has ramifications for rapidly dividing tissue in particular and therefore underlies the fetal developmental disorders and megaloblastic anemia (alongside aspects of neuronal dysfunction), associated with either folate or vitamin B12 deficiency [,,].
  • The efficient functioning of the folate cycle is also necessary for the synthesis and regeneration of tetrahydrobiopterin, an essential cofactor for the enzymes that convert amino acids to both monoamine neurotransmitters (serotonin, melatonin, dopamine, noradrenaline, adrenaline), and nitric oxide [,]

Functions of Vitamin B Complex/B vitamins

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Vitamin Name Structure Molecular Function
Vitamin B1 thiamine Thiamine plays a central role in the release of energy from carbohydrates. It is involved in RNA and DNA production, as well as nerve function. Its active form is a coenzyme called thiamine pyrophosphate (TPP), which takes part in the conversion of pyruvate to acetyl coenzyme A in metabolism.
Vitamin B2 riboflavin Riboflavin is involved in release of energy in the electron transport chain, the citric acid cycle, as well as the catabolism of fatty acids (beta oxidation)..
Vitamin B3 niacin
Niacin is composed of two structures: nicotinic acid and nicotinamide. There are two co-enzyme forms of niacin: nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). Both play an important role in energy transfer reactions in the metabolism of glucose, fat and alcohol.NAD carries hydrogens and their electrons during metabolic reactions, including the pathway from the citric acid cycle to the electron transport chain. NADP is a coenzyme in lipid and nucleic acid synthesis.
Vitamin B5 pantothenic acid Pantothenic acid is involved in the oxidation of fatty acids and carbohydrates. Coenzyme A, which can be synthesized from pantothenic acid, is involved in the synthesis of amino acids, fatty acids, ketone bodies, cholesterol,[5] phospholipids, steroid hormones, neurotransmitters (such as acetylcholine), and antibodies.[6]
Vitamin B6 pyridoxine, pyridoxal, pyridoxamine The active form pyridoxal 5′-phosphate (PLP) (depicted) serves as a cofactor in many enzyme reactions mainly in amino acid metabolism including biosynthesis of neurotransmitters.
Vitamin B7 biotin Biotin plays a key role in the metabolism of lipids, proteins and carbohydrates. It is a critical co-enzyme of four carboxylases: acetyl CoA carboxylase, which is involved in the synthesis of fatty acids from acetate; pyruvate CoA carboxylase, involved in gluconeogenesis; β-methylcrotonyl CoA carboxylase, involved in the metabolism of leucine; and propionyl CoA carboxylase, which is involved in the metabolism of energy, amino acids and cholesterol.
Vitamin B9 folate Folate acts as a co-enzyme in the form of tetrahydrofolate (THF), which is involved in the transfer of single-carbon units in the metabolism of nucleic acids and amino acids. THF is involved in pyrimidine nucleotide synthesis, so is needed for normal cell division, especially during pregnancy and infancy, which are times of rapid growth. Folate also aids in erythropoiesis, the production of red blood cells.
Vitamin B12 cobalamin Vitamin B12 is involved in the cellular metabolism of carbohydrates, proteins and lipids. It is essential in the production of blood cells in bone marrow, and for nerve sheaths and proteins. Vitamin B12 functions as a co-enzyme in intermediary metabolism for the methionine synthase reaction with methylcobalamin, and the methylmalonyl CoA mutase reaction with adenosylcobalamin

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Deficiency Symptoms of Vitamin B Complex/B vitamins

Several named vitamin deficiency diseases may result from the lack of sufficient B vitamins. Deficiencies of other B vitamins result in symptoms that are not part of a named deficiency disease.

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Vitamin Name Deficiency effects
Vitamin B1 thiamine Deficiency causes beriberi. Symptoms of this disease of the nervous system include weight loss, emotional disturbances, Wernicke encephalopathy (impaired sensory perception), weakness and pain in the limbs, periods of irregular heartbeat, and edema (swelling of bodily tissues). Heart failure and death may occur in advanced cases. Chronic thiamin deficiency can also cause alcoholic Korsakoff syndrome, irreversible dementia characterized by amnesia and compensatory confabulation.
Vitamin B2 riboflavin
Main article: Riboflavin § Deficiency

Deficiency causes ariboflavinosis. Symptoms may include cheilosis (cracks in the lips), high sensitivity to sunlight, angular cheilitis, glossitis (inflammation of the tongue), seborrheic dermatitis or pseudo-syphilis (particularly affecting the scrotum or labia majora and the mouth), pharyngitis (sore throat), hyperemia, and edema of the pharyngeal and oral mucosa.
Vitamin B3 niacin Deficiency, along with a deficiency of tryptophan causes pellagra. Symptoms include aggression, dermatitis, insomnia, weakness, mental confusion, and diarrhea. In advanced cases, pellagra may lead to dementia and death (the 3(+1) D’s: dermatitis, diarrhea, dementia, and death).
Vitamin B5 pantothenic acid Deficiency can result in acne and paresthesia, although it is uncommon.
Vitamin B6 pyridoxine, pyridoxal, pyridoxamine
Main article: Vitamin B6 § Deficiency

seborrhoeic dermatitis-like eruptions, pink eye, neurological symptoms (e.g. epilepsy)
Vitamin B7 biotin Deficiency does not typically cause symptoms in adults but may lead to impaired growth and neurological disorders in infants. Multiple carboxylase deficiency, an inborn error of metabolism, can lead to biotin deficiency even when dietary biotin intake is normal.
Vitamin B9 folic acid Deficiency results in macrocytic anemia, and elevated levels of homocysteine. Deficiency in pregnant women can lead to birth defects.
Vitamin B12 cobalamin Deficiency results in macrocytic anemia, elevated methylmalonic acid and homocysteine, peripheral neuropathy, memory loss, and other cognitive deficits. It is most likely to occur among elderly people, as absorption through the gut declines with age; the autoimmune disease pernicious anemia is another common cause. It can also cause symptoms of mania and psychosis. In rare extreme cases, paralysis can result.

The B vitamins: nomenclature, dietary sources, coenzyme forms (roles), symptoms of deficiency, and risk factors (over and above low consumption).

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Health Benefit of Vitamin B Complex/B vitamins


Thiamine (B1)

  • Vitamin B1, also known as thiamine, ensures that the body can produce new, healthy cells. It has also been reported to possess anti-stress properties, in addition to the ability to boost your immune system when it’s low. Vitamin B1 is also essential for the breakdown of simple carbohydrates.

Thiamine (Vitamin B1) Foods

  • Vitamin B2, also known as riboflavin, helps to get rid of particles in the body which can damage our cells. B2 has also been linked with the potential prevention of early aging, in addition to the ability to reduce your risk of heart disease.
  • Furthermore, B2 is essential for the production of red blood cells and hemoglobin, which is responsible for ensuring that the rest of your body’s cells receive the oxygen that they require. There have also been studies [1] that suggest that vitamin B2 can help in overcoming migraines, however, the results are not conclusive.

Riboflavin (Vitamin B2) Foods

Almonds, rice, eggs, milk, yoghurt, spinach, soy and sprouts.

Niacin (B3)

  • One of the main roles of vitamin B3, also known as niacin, is to increase the levels of high-density lipoproteins (HDL) in the blood. These are the ‘good cholesterol’. The higher your HDL levels are, the lower your overall cholesterol ratio is. This means you are seen as being at a lower risk of developing cardiovascular diseases (CVD).
  • Several studies have also shown that vitamin B3 may be able to treat skin conditions such as acne.

Niacin (Vitamin B3) Foods:

Milk, eggs, beans, green vegetables and red meat.

Pantothenic Acid (B5)

  • Vitamin B5, also known as pantothenic acid, can be found in many foods in small quantities. Its main responsibilities include breaking down fats and carbohydrates for energy, and the production of important hormones such as testosterone.

There have been studies [4] that show that vitamin B5 can have a positive effect on skin, reducing the signs of ageing and improving blemishes, redness and spots.

Pantothenic Acid (Vitamin B5) Foods

Eggs, meat, yogurt, beans, and legumes.

Pyridoxine (B6)

  • Pyridoxine, also known as vitamin B6, has several different qualities. Firstly, it works to regulate blood levels of homocysteine, which is an amino acid associated with heart disease. It also helps to body to produce hormones such as serotonin and melatonin, as well as norepinephrine. These are our sleep and stress hormones that alter mood and energy levels.
  • There have also been a number of studies [5] that suggest that vitamin B6 can improve the condition of patients suffering from arthritis.

Pyridoxine (Vitamin B6) Foods

Seeds, rice, salmon, tuna, turkey and chicken.

Biotin (B7)

  • Vitamin B7 (biotin), also known as the beauty vitamin, has several benefits in relation to appearance, as it has been linked with improving the appearance of skin, hair, and nails.
  • There have also been studies [6] that suggest that vitamin B7 can help to control blood glucose levels, suggesting that supplementation can be beneficial for those who suffer from diabetes. Biotin may also be beneficial during pregnancy to support the normal growth of the baby.

 

Biotin (Vitamin B7) Foods

  • Most commonly found in meats, such as chicken and pork, although it can also be found in egg yolks, potatoes and nuts.

Folate (B9)

  • Folate, also known as vitamin B9, has several key benefits. It has been linked [7] to the prevention of memory loss, as well as improving depression. It has also been strongly linked with the prevention of birth defects in babies.
  • B9 can be found in a synthetic form, folic acid, which is often added to foods such as cereals to fortify them. It can also be bought in supplement form.

Folic Acid (Vitamin B9) Foods

  • Can be consumed naturally through green leafy vegetables, asparagus, root vegetables, milk, wheat, beans and salmon.

Cobalamin (B12)

  • The main role of vitamin B12 is to aid the other B vitamins in completing their roles. It works with folate to produce red blood cells, as well as to produce haemoglobin.
  • Vitamin B12 is only found in animal products, which means the vegans and vegetarians are at risk of being deficient. It may be necessary to supplement with vitamin B12 if you do not consume many animal products.

Cobalamin (Vitamin B12) Foods

  • Vitamin B12 most commonly found in fish, pork, beef, dairy and eggs.

Mood

  • B-complex vitamins have been known since the 1940s as antistress nutrients. Many of the vitamins have direct effects on mood and perception. For example, vitamin B1 supplements improve overall mood; high doses of vitamin B3 (in combination with vitamin C) have been used successfully to treat recent-onset schizophrenia. Vitamin B6 is needed to make serotonin, a neurotransmitter with antidepressant benefits.

Blood sugar.

  • Biotin and vitamin B1 stand out for their roles in maintaining normal blood sugar levels. Your body needs biotin to make insulin, a hormone that controls blood sugar levels. In addition, biotin regulates genes involved in the metabolism of glucose, amino acids, and fatty acids. Large amounts of biotin can lower triglyceride levels, and a combination of biotin and chromium picolinate has been shown to lower blood sugar levels. Vitamin B1 (100 mg, three times daily) has been shown to lower levels of microalbuminuria (protein in urine) in people with type 2 diabetes.

Cognitive function.

Approximately one-third of seniors suffer from atrophic gastritis, a condition that interferes with vitamin B12 absorption. Studies have found that vitamin B12 deficiency can mimic Alzheimer’s disease and other types of dementia. In these cases, taking vitamin B12 can restore cognitive function. Other B-complex vitamins, including niacin and folic acid, may be helpful in combination with vitamin B12.

Macular degeneration.

Researchers reported in the February 2009 issue of Archives of Internal Medicine that large supplemental amounts of B-complex vitamins led to a 35 percent lower incidence risk of age-related macular degeneration in women over the course of seven years.

Balancing Stress

  • The B vitamins are vital cofactors for specific enzymes involved in the production of adrenal hormones. These hormones regulate many processes in your body as well as help you to adapt to stress and cope with anxiety.
  • Your adrenal response to stress causes the metabolism of your cells to speed up, increasing the number of nutrients needed, which can lead to deficiencies. According to research, chronic stress depletes vitamin B6, so supplementing to maintain healthy levels could be of help therapeutically.

Bending and Stretching

  • Research has indicated that Vitamin B3 may have anti-inflammatory properties that could offer protection against arthritic symptoms and the need for pharmaceutical anti-inflammatory drugs.
  • Additionally, vitamin B5 may be of help to sufferers of Rheumatoid Arthritis, as these individuals have been found to have lower levels of this B vitamin in their blood than healthy people.
  • Scientists discovered that the lower the levels of B5, the more extreme the symptoms were. Further studies have shown that vitamin B5 may improve the morning stiffness and pain associated with rheumatoid arthritis.

Brighter Vision

  • Over time eye health can deteriorate leaving some people with short-sightedness and others with cataracts or age-related macular degeneration (AMD), which can lead to blindness. Fortunately, vitamin B2 (Riboflavin) works in tandem with other nutrients to help maintain normal clear vision.
  • Animal trials show that rats fed riboflavin deficient diets have developed cataracts and other studies have led some researchers to conclude that riboflavin deficiency may also contribute to night blindness.

Pregnant or Breastfeeding Women

  • During pregnancy, the demand for B vitamins, particularly B12 and folate, grows to support fetal development .
  • In women who are pregnant or breastfeeding, especially those who follow vegetarian or vegan diets, supplementing with a B-complex vitamin is crucial.
  • B12 or folate deficiency in pregnant or breastfeeding women can lead to severe neurological damage or birth defects in the fetus or infant .

Cardiovascular disease

  • Low levels of folic acid (and sometimes low B6 and B12 levels) lead to increases in blood levels of homocysteine, a chemical that damages blood vessel walls and sets the stage for cholesterol deposits.
  • Recently, researchers at the University of Southern California gave subjects high-dose B-complex vitamins or placebos daily for three years. Those taking the vitamins had significantly less thickening of their blood vessel walls, according to an article in Stroke.

Related Compounds

Many of the following substances have been referred to as vitamins as they were once believed to be vitamins. They are no longer considered as such, and the numbers that were assigned to them now form the “gaps” in the true series of B-complex vitamins described above (e.g., there is no vitamin B4). Some of them, though not essential to humans, are essential in the diets of other organisms; others have no known nutritional value and may even be toxic under certain conditions.

  • Vitamin B4 – can refer to the distinct chemicals choline, adenine, or carnitine.[rx][rx] Choline is synthesized by the human body, but not sufficient to maintain good health, and is now considered an essential dietary nutrient.[rx] Adenine is a nucleobase synthesized by the human body.[rx] Carnitine is an essential dietary nutrient for certain worms, but not for humans.[rx]
  • Vitamin B8 – adenosine monophosphate (AMP), also known as adenylic acid.[rx] Vitamin B8 may also refer to inositol.[rx]
  • Vitamin B10 –  para-aminobenzoic acid (PABA or PABA), a chemical component of the folate molecule produced by plants and bacteria, and found in many foods.[rx][rx] It is best known as a UV-blocking sunscreen applied to the skin and is sometimes taken orally for certain medical conditions.[rx][rx]
  • Vitamin B11 –  pteryl-hepta-glutamic acid (PHGA; chick growth factor). Vitamin Bc-conjugate was also found to be identical to PHGA.
  • Vitamin B13 –  orotic acid.[rx]
  • Vitamin B14 – cell proliferant, anti-anemia, rat growth factor, and antitumor pterin phosphate named by Earl R. Norris. Isolated from human urine at 0.33ppm (later in the blood), but later abandoned by him as further evidence did not confirm this. He also claimed this was not xanthopterin.
  • Vitamin B15 –  pangamic acid,[rx] also known as pangamate. Promoted in various forms as a dietary supplement and drug; considered unsafe and subject to seizure by the US Food and Drug Administration.[rx]
  • Vitamin B16 –  dimethylglycine (DMG)[rx] is synthesized by the human body from choline.
  • Vitamin B17 – the pseudoscientific name for the poisonous compound amygdalin, also known as the equally pseudoscientific name “nitrilosides” despite the fact that it is a single compound. Amygdalin can be found in various plants but is most commonly extracted from apricot pits and other similar fruit kernels. Amygdalin is hydrolyzed by various intestinal enzymes to form, among other things, hydrogen cyanide, which is toxic to human beings when exposed to a high enough dosage. Some proponents claim that amygdalin is effective in cancer treatment and prevention, despite its toxicity and a severe lack of scientific evidence.[rx]
  • Vitamin B20  – L-carnitine.[rx]
  • Vitamin Bf  – carnitine.[rx]
  • Vitamin Bm – Myo-inositol, also called “mouse antialopaecia factor”.[rx]
  • Vitamin Bp – “antiperosis factor”, which prevents persons, a leg disorder, in chicks; can be replaced by choline and manganese salts.[rx][rx][rx]
  • Vitamin BT: carnitine.[rx][rx]
  • Vitamin Bv – a type of B6 other than pyridoxine.
  • Vitamin BW – a type of biotin other than d-biotin.
  • Vitamin Bx – an alternative name for both pABA (see vitamin B10) and pantothenic acid.[rx][rx]


References

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Vitamin A; Types, Deficiency Symptoms, Food Source, Health Benefit

Vitamin A is a group of unsaturated nutritional organic compounds that includes retinol, retinal, retinoic acid, and several provitamins A carotenoids (most notable beta-carotene). Vitamin A has multiple functions: it is important for growth and development, for the maintenance of the immune system and good vision. Vitamin A is needed by the retina of the eye in the form of retinal, which combines with protein opsin to form rhodopsin, the light-absorbing molecule necessary for both low-light (scotopic vision) and color vision.  Vitamin A also functions in a very different role as retinoic acid (an irreversibly oxidized form of retinol), which is an important hormone-like growth factor for epithelial and other cells.

Vitamin A is a fat-soluble vitamin that is essential for humans and other vertebrates. Vitamin A comprises a family of molecules containing a 20 carbon structure with a methyl-substituted cyclohexenyl ring (beta-ionone ring) and a tetraene side chain with a hydroxyl group (retinol), aldehyde group (retinal), carboxylic acid group (retinoic acid), or ester group (retinyl ester) at carbon-15. The term vitamin A includes provitamin A carotenoids that are dietary precursors of retinol. The term retinoids refer to retinol, its metabolites, and synthetic analogs that have a similar structure. Carotenoids are polyisoprenoids, of which more than 600 forms exist. Of the many carotenoids in nature, several have provitamin A nutritional activity, but food composition data are available for only three (α-carotene, β-carotene, and β-cryptoxanthin) [rx].

How much vitamin A do I need?

The amount of vitamin A adults (19-64 years) need is:

  • 0.7mg a day for men
  • 0.6mg a day for women

Vitamin A can be found in two principal forms in foods

  • Retinol, the form of vitamin A absorbed when eating animal food sources, is a yellow, fat-soluble substance. Since the pure alcohol form is unstable, the vitamin is found in tissues in a form of retinyl ester. It is also commercially produced and administered as esters such as retinyl acetate or palmitate.
  • The carotenes alpha-carotene, beta-carotene, gamma-carotene; and the xanthophyll beta-cryptoxanthin (all of which contain beta-ionone rings), but no other carotenoids, function as provitamin A in herbivores and omnivore animals, which possess the enzyme beta-carotene 15,15′-dioxygenase which cleaves beta-carotene in the intestinal mucosa and converts it to retinol.

The three forms of active preformed vitamin A differ in purpose within the body and in their oxidation levels.

  • Retinol – Also known as vitamin A1. This is common in supplements and also associated with vitamin A toxicity in extremely high doses.
  • Retinal – Essential to your vision, this form of vitamin A converts light into electrical input to your brain.
  • Retinoic acid – Retinoic acid is critical in cell differentiation. When your cells are very young and still not sure if they will become eye cells, heart cells or brain cells, they depend on retinoic acid to tell them what to turn into.

Deficiency Symptoms of Vitamin A

  • Night Blindness  – Low levels of vitamin A can cause a lack of rhodopsin, which is a light-sensitive protein present in your eye. And the lack of this protein impairs vision in dim light. You may, therefore, find it difficult to see properly at night when you have vitamin A deficiency. Watch out for telltale signs like difficulty driving at night. Night blindness is harder to notice in children because they may not know enough to complain about it. As a parent, have you noticed your child behaves differently once there’s no light or when they are in a dark room? If the child is inactive or apprehensive about moving around, probe further.
  • Dry Eyes  –  Changes in the way you see are usually the first and most prominent sign of vitamin A deficiency. “Xerophthalmia” is the term used to indicate the range of eye problems triggered by vitamin A deficiency.ated can point to a vitamin A deficiency.
  • Dry Skin, Rashes, Broken Nails – Fatigue or constant tiredness may be another early sign. Though it may seem non-specific, like itching or dry skin, probe further, especially if there are clear eye-related symptoms accompanying these
  • White Or Silver Gray Foamy Spots In The Eye – Another sign of a vitamin A deficiency is the formation of foamy spots known as Bitot’s spots in the whites of your eyes. Bitot’s spots can be triangular or irregular in shape and usually appear at the 3 o’clock or 9 o’clock positions. They will appear slightly raised and look more like skin rather than a mucous membrane. They are essentially formed from a buildup of keratin because of the drying out of the cornea.
  • Corneal Ulcers And Blindness – Without proper treatment, a deficiency in vitamin A can lead to the development of sores or ulcers in the eyes. An ulcer in the eye may look like a tiny punched-out area or have a fluffy appearance. Eventually, damage to the eyes can result in blindness. In fact, vitamin A deficiency is the main cause of preventable blindness in children – but one that is more commonly observed in the developing world.
  • Frequent Infections – Frequent throat, chest, bladder, or stomach infections accompanied by eye problems may indicate a vitamin A deficiency. Vitamin A has earned the name “the anti-infective vitamin” because of its vital role in the proper functioning of the immune system. Your skin and the mucosal cells which line your urinary tract, digestive tract, and airways function as a barrier and first line of defense against infection.
  • Growth Retardation In Children – In children with severe vitamin A deficiency, normal growth and development can slow down.
  • Poor eye health
  • Chronic gut
  • Dry, thick or scaling skin
  • Macular degeneration
  • Dry mucous membranes
  • Weak fingernails
  • Low vitamin D levels
  • Respiratory infections
  • Immune system dysfunction
  • Leaky gut or other gut health issues
  • Autoimmune disease
  • Excessive sun exposure
  • Vegetarian diet
  • Low-fat diet
  • Being a woman of childbearing age
  • Having cystic fibrosis

Food Sources of Vitamin A

Carrots are a source of vitamin A

Vitamin A is found in many foods, including the following list. Bracketed values are retinol activity equivalences (RAEs) and percentage of the adult male RDA, per 100 grams of the foodstuff (average). Conversion of carotene to retinol varies from person to person and bioavailability of carotene in food varies.

  • Cod liver oil (30000 μg 3333%)
  • Liver (turkey) (8058 μg 895%)
  • Liver (beef, pork, fish) (6500 μg 722%)
  • Liver (chicken) (3296 μg 366%)
  • Ghee (3069 μg 344%)
  • Sweet potato (961 μg 107%)
  • Carrot (835 μg 93%)
  • Broccoli leaf (800 μg 89%)
  • Butter (684 μg 76%)
  • Kale (681 μg 76%)
  • Collard greens (frozen then boiled) (575 μg 64%)
  • Butternut squash (532 μg 67%)
  • Dandelion greens (508 μg 56%)
  • Spinach (469 μg 52%)
  • Pumpkin (426 μg 43%)
  • Collard greens (333 μg 37%)
  • Cheddar cheese (265 μg 29%)
  • Cantaloupe melon (169 μg 19%)
  • Bell pepper/capsicum, red (157 μg 17%)
  • Egg (140 μg 16%)
  • Apricot (96 μg 11%)
  • Papaya (55 μg 6%)
  • Tomatoes (42 μg 5%)
  • Mango (38 μg 4%)
  • Pea (38 μg 4%)
  • Broccoli florets (31 μg 3%)
  • Milk (28 μg 3%)
  • Bell pepper/capsicum, green (18 μg 2%)
  • Spirulina (3 μg 0.3%)

Recommended Intakes

Intake recommendations for vitamin A and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the Institute of Medicine of the National Academies (formerly National Academy of Sciences) [rx]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and gender, include:

  • Recommended Dietary Allowance (RDA) – Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals.
  • Adequate Intake (AI) – Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA.
  • Estimated Average Requirement (EAR) – Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals.
  • Tolerable Upper Intake Level (UL) –  Maximum daily intake unlikely to cause adverse health effects.

RDAs for vitamin A are given as mcg of retinol activity equivalents (RAE) to account for the different bioactivities of retinol and provitamin A carotenoids (see Table 1). Because the body converts all dietary sources of vitamin A into retinol, 1 mcg of physiologically available retinol is equivalent to the following amounts from dietary sources: 1 mcg of retinol, 12 mcg of beta-carotene, and 24 mcg of alpha-carotene or beta-cryptoxanthin. From dietary supplements, the body converts 2 mcg of beta-carotene to 1 mcg of retinol.

Currently, vitamin A is listed on food and supplement labels in international units (IUs) even though nutrition scientists rarely use this measure. Conversion rates between mcg RAE and IU are as follows [rx]

  • 1 IU retinol = 0.3 mcg RAE
  • 1 IU beta-carotene from dietary supplements = 0.15 mcg RAE
  • 1 IU beta-carotene from food = 0.05 mcg RAE
  • 1 IU alpha-carotene or beta-cryptoxanthin = 0.025 mcg RAE

However, under FDA’s new labeling regulations for foods and dietary supplements that take effect by January 1, 2020 (for companies with annual sales of $10 million or more) or January 1, 2021 (for smaller companies), vitamin A will be listed only in mcg RAE and not IUs [rx,rx].

An RAE cannot be directly converted into an IU without knowing the source(s) of vitamin A. For example, the RDA of 900 mcg RAE for adolescent and adult men is equivalent to 3,000 IU if the food or supplement source is preformed vitamin A (retinol). However, this RDA is also equivalent to 6,000 IU of beta-carotene from supplements, 18,000 IU of beta-carotene from food, or 36,000 IU of alpha-carotene or beta-cryptoxanthin from food. So a mixed diet containing 900 mcg RAE provides between 3,000 and 36,000 IU of vitamin A, depending on the foods consumed.

[stextbox id=’info’]

Life stage
group		 U.S. RDAs or
Adequate Intakes, AI,
retinol activity equivalents (μg/day)		 Upper limits,
UL* (μg/day)
Infants 0–6 months 400 (AI) 500 (AI)
7–12 months 600 600
Children 1–3 years 300 600
4–8 years 400 900
Males 9–13 years 600 1700
14–18 years 900 2800
>19 years 900 3000
Females 9–13 years 600 1700
14–18 years 700 2800
>19 years 700 3000
Pregnancy <19 years 750 2800
>19 years 770 3000
Lactation <19 years 1200 2800
>19 years 1300 3000
  • ULs are for natural and synthetic retinol ester forms of vitamin A. Beta-carotene and other provitamin A carotenoids from foods and dietary supplements are not added when calculating total vitamin A intake for safety assessments, although they are included as RAEs for RDA and AI calculations.[rx][rx]
 
Age Male Female Pregnancy Lactation
0–6 months* 400 mcg RAE 400 mcg RAE
7–12 months* 500 mcg RAE 500 mcg RAE
1–3 years 300 mcg RAE 300 mcg RAE
4–8 years 400 mcg RAE 400 mcg RAE
9–13 years 600 mcg RAE 600 mcg RAE
14–18 years 900 mcg RAE 700 mcg RAE 750 mcg RAE 1,200 mcg RAE
19–50 years 900 mcg RAE 700 mcg RAE 770 mcg RAE 1,300 mcg RAE
51+ years 900 mcg RAE 700 mcg RAE

* Adequate Intake (AI), equivalent to the mean intake of vitamin A in healthy, breastfed infants.

[/stextbox]

Health Benefits of Vitamin A

Essential for Good Eyesight

  • Your eyes are delicate and hence require extra care and protection. Vitamin A is widely known to treat weak eyesight, keeping the eyes nice and moist. It is also evident that regular consumption of vitamin A enhances night vision preventing you from night blindness. According to eye specialists, retinol is the only nutrient that helps the development of ‘visual purple’ in your eyes. You will be delighted to know that vitamin A has the potential to reduce risks of cataracts and macular degeneration, which are age-related eye problems.

It Prevents Urinary Stones

  • Urinary stones are a troublesome health problem. You should try every possible precaution to avoid it. However, an effective way of steering clear of the health complication is to consume a diet rich in vitamin A. It is known to work as a shield against factors that form urinary calculi by producing calcium phosphate in your body. Vitamin A also keeps the urinary tract in shape that minimizes the chance of urinary stone reoccurrence.

For Healthy Bones

  • Dairy products and vitamin D are known to keep your bones and teeth stronger. This is why experts recommend incorporating dairy products into your routine and drinking a glass of milk regularly to avoid bones problems. After thorough research and spending considerable time, scientists have found that regular consumption of vitamin A is effective for your bones and teeth as well. Combined with other nutrients, vitamin A produces a solid layer called dentin below the surface of your teeth. This layer strengthens your teeth against various oral health problems.

It Promotes Muscle Growth

  • You might not pay attention to it, but muscle growth is essential specifically for children and growing teens. An accurate diet ensures proper muscle growth. Since vitamin A contains a lot of health benefits, promoting better muscle growth is it’s another health benefit. For proper muscle growth of children and growing teens, it is important to incorporate food items into their diet that contains plenty of vitamin A, which will help prevent the development of muscular dystrophy in the muscles.

Vitamin A Repairs Tissue

  • Your body reproduces tissues and cells naturally, but it needs nutrients for the process. Without enough nutrients, this process can’t take place and your body remains unable to produce new tissues. Therefore, consume vitamin A in any form to enable this natural process as it replaces old tissues with the new ones effectively.

It Treats Measles

  • Measles is neither rare nor a frequently occurring disease, but it is indeed draining. Child specialists suggest that children who are vitamin A deficient fall prey to measles. Hence, the solution is to incorporate food items that contain vitamin A into their diets. An adequate amount of this vitamin will relieve diarrhea and fever that comes with measles.

Vitamin A Delays Aging

  • An occurrence of fine lines and wrinkles are common as you age. Although there are a number of treatments and products available to reduce these signs of aging, they cannot do what a nutrient can do. This is why beauty experts trust vitamin A. It is said to delay aging by reducing fine lines and wrinkles. Since it naturally contains moisture, it keeps your skin moist. When your skin absorbs this moisture, it becomes youthful again.

For Acne

  • Excessive sebum production cause acne, which is stressing as it might take months to heal. Taking vitamin A supplements are said to treat acne by limiting sebum production on the skin. The antioxidants in the vitamin rejuvenate dead skin cells leaving in smooth and baby soft.

It Strengthens Immune system

  • Vitamin A works as an immunity booster. A powerful immune system keeps infectious bacteria at bay, but you need to maintain its functionality. Consuming vitamin A on a daily basis is said to increase lymphocytic responses that fight disease-causing antigens. It has properties that are necessary to keep mucus membranes moist. This moist mucus membrane ensures better immunity and promotes the activity of white blood cells. This process also prevents reentrance of germs and bacteria in your body.

For High Cholesterol

  • High cholesterol levels are daunting due to their contribution to various cardio problems. There are numerous other severe health issues associated with high cholesterol. This is why nutritionists suggest diets loaded with vitamin A because it helps lower high levels of cholesterol. It is also known to widen arteries to ensure proper blood flow. Vitamin A can reduce the chances of blood clotting as well.

For Skin

  • All the vitamins are known to enhance the condition of skin – so does vitamin A. It has antioxidants and healing properties that are essential for your skin health. Consuming vitamin A enriched diet improves skin discoloration giving it a natural glow.

Boosts Bone Health

  • This essential vitamin strengthens bones and teeth. Vitamin A helps in the formation of dentin, a layer of hard material just below the surface of the teeth, thereby enhancing its strength.

Prevents Urinary Stones

  • Vitamin A prevents the formation of urinary calculi due to the formation of calcium phosphate. It also helps keep the lining of the urinary tract in shape, thereby reducing the recurring chance of stones.

Promotes Muscle Growth

  • By keeping the bones healthy and retaining their shape, vitamin A plays an essential role in ensuring proper muscle growth in children and growing teens, thereby preventing the chances of developing muscular dystrophy.

Reduces Risk of Acne

  • Vitamin A helps cut down excess sebum production, thereby reducing the risk of acne. It also reinforces the protective tissues of the skin, thereby enhancing the overall health and vitality of the skin surface. It is also essential for the proper maintenance of the skin tissues and mucous membranes. It flushes out the toxins from your body and cleanses the system by virtue of its antioxidant properties.

Prevents Cancer

  • Vitamin A is also a powerful antioxidant, which can prevent certain forms of cancer.

Repairs Tissues

  • Vitamin A plays an important role in replacing old and worn out tissues with new ones, as well as in keeping your bones and teeth strong.

Slows Aging

  • Vitamin A is famous for its wrinkle-eliminating properties, which can reduce age spots and fine lines. It can slow down the aging process by enhancing the overall health of the skin.

Treats Measles

  • Deficiency of vitamin A may cause measles in children.  Intake of foods rich in this vitamin helps relieve the fever and diarrhea caused by measles.

Metabolic functions

Vitamin A plays a role in a variety of functions throughout the body, such as:

  • Vision
  • Gene transcription
  • Immune function
  • Embryonic development and reproduction
  • Bone metabolism
  • Hematopoiesis
  • Skin and cellular health
  • Teeth
  • Mucous membrane

Resources


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Bethanechol; Indications, Dosage, Side Effects, Interactions ,Pregnancy

Bethanechol is a slowly hydrolyzing muscarinic agonist with no nicotinic effects. Bethanechol is generally used to increase smooth muscle tone, as in the GI tract following abdominal surgery or in urinary retention in the absence of obstruction. It may cause hypotension,[1]

Bethanechol is a synthetic ester structurally and pharmacologically related to acetylcholine. A slowly hydrolyzed muscarinic agonist with no nicotinic effects, bethanechol is generally used to increase smooth muscle tone, as in the GI tract following abdominal surgery or in urinary retention in the absence of obstruction. It may cause hypotension, cardiac rate changes, and bronchial spasms.

Mechanism of Action of Bethanechol

Bethanechol directly stimulates cholinergic receptors in the parasympathetic nervous system while stimulating the ganglia to a lesser extent. Its effects are predominantly muscarinic, inducing the little effect on nicotinic receptors and negligible effects on the cardiovascular system.
Bethanechol is a parasympathomimetic (cholinergic) used for the treatment of acute postoperative and postpartum nonobstructive (functional) urinary retention and for neurogenic atony of the urinary bladder with retention. Bethanechol, a cholinergic agent, is a synthetic ester which is structurally and pharmacologically related to acetylcholine. It increases the tone of the detrusor urinae muscle, usually producing a contraction sufficiently strong to initiate micturition and empty the bladder. It stimulates gastric motility, increases gastric tone, and often restores impaired rhythmic peristalsis. Bethanechol chloride is not destroyed by cholinesterase and its effects are more prolonged than those of acetytcholine.

Indications of Bethanechol

Contra-Indications of Bethanechol

Dosage of Bethanechol

Strengths: 5 mg; 10 mg; 25 mg; 50 mg; 5 mg/mL

Urinary Retention

  • Initial dose: 5 to 10 mg orally once to obtain minimum effective dose; repeat the same amount at hourly intervals until satisfactory response occurs or a maximum of 50 mg has been given
  • Maintenance dose: 10 to 50 mg orally 3 to 4 times a day

Neurogenic Bladder

  • Initial dose: 5 to 10 mg orally once to obtain minimum effective dose; repeat the same amount at hourly intervals until satisfactory response occurs or a maximum of 50 mg has been given
  • Maintenance dose: 10 to 50 mg orally 3 to 4 times a day

Side Effects of Bethanechol

The most common 

More common

Less common

Drug Interactions of Bethanechol

Bethanechol may interact with the following drugs,supplyment & may change the efficacy of drugs

Pregnancy & Lactation of Bethanechol

FDA Pregnancy Category C

Pregnancy

This medication should not be used during pregnancy unless the benefits outweigh the risks. If you become pregnant while taking this medication, contact your doctor immediately.

Lactation

It is not known if bethanechol chloride passes into breast milk. If you are a breast-feeding mother and are taking this medication, it may affect your baby. Talk to your doctor about whether you should continue breast-feeding. The safety and effectiveness of using this medication have not been established for children.

References

  1. https://pubchem.ncbi.nlm.nih.gov/compound/bethanechol
  2. DrugBank
  3. http://www.drugbank.ca/drugs/DB01019
  4. http://www.drugbank.ca/drugs/DB01019#targets
  5. https://comptox.epa.gov/dashboard/dsstoxdb/results?search=DTXSID5048398
  6. https://www.drugs.com/mtm/bethanechol.html
  7. https://www.fda.gov/Drugs/InformationOnDrugs/ucm129662.htm
  8. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0000243/
  9. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0009282/
  10. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0009283/
  11. https://www.whocc.no/atc/
  12. https://en.wikipedia.org/wiki/Bethanechol
  13. https://pubchem.ncbi.nlm.nih.gov
  14. https://www.webmd.com/drugs/2/drug-10669/bethanechol-chloride-subcutaneous/details/list-contraindications
  15. MeSH
    https://www.ncbi.nlm.nih.gov/mesh/68018723

    http://www.nlm.nih.gov/mesh/meshhome.html
    https://www.ncbi.nlm.nih.gov/mesh/68010277
    https://www.ncbi.nlm.nih.gov/mesh/68018721

    http://www.ebi.ac.uk/chebi/userManualForward.do#ChEBI%20Ontology

    https://www.ncbi.nlm.nih.gov/projects/linkout

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Metoclopramide; Indications, Uses, Dosage, Side Effects, Interactions ,Pregnancy

Metoclopramide is a substituted benzamide and a derivative of para-aminobenzoic acid (PABA) that is structurally related to procainamide, with gastroprokinetic and antiemetic effects. Metoclopramide exerts its prokinetic effect by antagonizing dopamine-mediated relaxation effect on gastrointestinal smooth muscle. This enhances the response of the gastrointestinal smooth muscle to cholinergic stimulation, thereby leading to an increase of gastric emptying into the intestines. Metoclopramide may also strengthen the lower esophagus sphincter, thereby preventing acid reflux. This agent antagonizes D2 dopamine receptors in the chemoreceptive trigger zone (CTZ) of the medulla, thereby preventing nausea and vomiting.

Mechanism of Action of Metoclopramide

Metoclopramide inhibits gastric smooth muscle relaxation produced by dopamine, therefore increasing the cholinergic response of the gastrointestinal smooth muscle. It accelerates intestinal transit and gastric emptying by preventing relaxation of the gastric body and increasing the phasic activity of tantrum. Simultaneously, this action is accompanied by relaxation of the upper small intestine, resulting in an improved coordination between the body and antrum of the stomach and the upper small intestine. Metoclopramide also decreases reflux into the esophagus by increasing the resting pressure of the lower esophageal sphincter and improves acid clearance from the esophagus by increasing amplitude of esophageal peristaltic contractions. Metoclopramide’s dopamine antagonist action raises the threshold of activity in the chemoreceptor trigger zone and decreases the input from afferent visceral nerves. Studies have also shown that high doses of metoclopramide can antagonize 5-hydroxytryptamine (5-HT) receptors in the peripheral nervous system in animals.

 

Or

Metoclopramide is a potent dopamine-receptor antagonist, and some of the actions of metoclopramide on GI smooth muscle may be mediated via antagonism of dopaminergic neurotransmission, Specific dopamine receptors in the esophagus and stomach have been identified; however, it is not known if there is a dopaminergic control system for smooth muscle function in the upper GI tract. In the GI tract, dopamine is principally an inhibitory neurotransmitter. Dopamine decreases the intensity of esophageal contractions, relaxes the proximal stomach, and reduces gastric secretion. Although metoclopramide blocks these inhibitory effects of dopamine, the actual role of dopamine in the peripheral control of GI motility has not been fully elucidated. Since cholinergic mechanisms are responsible for most excitatory motor activity in the GI tract, it appears that metoclopramide’s therapeutic effects are principally caused by the drug’s cholinergic-like activity; however, antagonism of GI dopaminergic activity may augment metoclopramide’s cholinergic-like activity

or

Metoclopramide is a potent central dopamine-receptor antagonist. The drug has antiemetic and sedative activity. The precise mechanism of antiemetic action of metoclopramide is unclear, but the drug has been shown to directly affect the medullary chemoreceptor trigger zone (CTZ) in the area postrema, apparently by blocking dopamine (e.g., D2) receptors in the CTZ. Metoclopramide increases the CTZ threshold and decreases the sensitivity of visceral nerves that transmit afferent impulses from the GI tract to the vomiting center in the lateral reticular formation. The drug also enhances gastric emptying, which is believed to minimize stasis that precedes vomiting. It also has been suggested that inhibition of serotonin (i.e., 5-HT3) receptors, at least when relatively high doses of metoclopramide are used, may contribute to the antiemetic action of the drug. Metoclopramide inhibits the central and peripheral emetic effects of apomorphine, hydergine, and levodopa.

Indications of Metoclopramide

Therapeutic Indications of Metoclopramide

The authorized indications for products are different but can broadly be grouped in the following way

Therapeutic Uses of Metoclopramide

  • Metoclopramide tablets are indicated as short-term (4 to 12 weeks) therapy for adults with symptomatic, documented gastroesophageal reflux who fail to respond to conventional therapy.
  • Metoclopramide tablets, USP is indicated for the relief of symptoms associated with acute and recurrent diabetic gastric stasis. The usual manifestations of delayed gastric emptying (eg, nausea, vomiting, heartburn, persistent fullness after meals, and anorexia) appear to respond to Metoclopramide Tablets within different time intervals. Significant relief of nausea occurs early and continues to improve over a three-week period. Relief of vomiting and anorexia may precede the relief of abdominal fullness by one week or more.
  • Metoclopramide injection is indicated for the prophylaxis of vomiting associated with emetogenic cancer chemotherapy.
  • Metoclopramide injection is indicated for the prophylaxis of postoperative nausea and vomiting in those circumstances where nasogastric suction is undesirable.
  • Metoclopramide injection may be used to facilitate small bowel intubation in adults and pediatric patients in whom the tube does not pass the pylorus with conventional maneuvers.
  • Metoclopramide injection may be used to stimulate gastric emptying and intestinal transit of bariumin cases where delayed emptying interferes with radiological examination of the stomach and/or small intestine.
  • Diamond-Blackfan anemia (DBA) is a congenital anemia characterized by a low reticulocyte count, the absence or severe reduction of hemoglobin-containing cells in the bone marrow, and normal megakaryocytic and granulocytic differentiation. Although the anemia may initially respond to corticosteroid therapy, many patients require lifelong red blood cell (RBC) transfusion, leading to infectious complications and iron overload.

Dosage

Strengths: 10 mg; 5 mg; 5 mg/5 mL; 5 mg/mL; 10 mg/mL

Gastroesophageal Reflux Disease

  • Symptomatic gastroesophageal reflux disease (GERD): 10 to 15 mg orally up to 4 times a day (30 minutes before meals and at bedtime), depending upon symptoms being treated and clinical response
  • Intermittent symptoms/at specific times of day: 20 mg orally once a day prior to provoking the situation
  • Use with esophageal erosions/ulcerations: 15 mg orally 4 times a day, if tolerated
  • Maximum dose: 60 mg/day
  • Maximum duration of therapy: 12 weeks

Nausea/Vomiting – Chemotherapy Induced

Parenteral

  • Initial dose: 1 to 2 mg/kg/dose (depending on the emetogenic potential of the agent) IV infused over a period of not less than 15 minutes, 30 minutes before administration of chemotherapy.
  • Subsequent doses: The dose should be repeated every 2 hours for 2 doses following the initial dose, then every 3 hours for 3 additional doses.
  • Parenteral: 10 to 20 mg IM at or near the end of surgery

Nausea/Vomiting – Postoperative

Parenteral

  • Initial dose: 1 to 2 mg/kg/dose (depending on the emetogenic potential of the agent) IV infused over a period of not less than 15 minutes, 30 minutes before administration of chemotherapy.
  • Subsequent doses: The dose should be repeated every 2 hours for 2 doses following the initial dose, then every 3 hours for 3 additional doses.

Small Intestine Intubation

  • If the tube has not passed the pylorus with conventional maneuvers in 10 minutes, a single undiluted dose may be administered via slow IV.
  • Parenteral: 10 mg IV metoclopramide base over a 1- to 2-minute period

Gastroparesis

  • Parenteral: 10 mg IV (slowly over a 1 to 2-minute period) or IM
  • Maximum duration of therapy: Up to 10 days
  • Oral: 10 mg orally 30 minutes before each meal and at bedtime for 2 to 8 weeks, depending upon response and the likelihood of continued well-being upon drug discontinuation
  • Maximum dose: 40 mg/day
  • Maximum duration of therapy: 12 weeks

Side Effects of Metoclopramide

The most common

Common

Rare

Drug Interactions of Metoclopramide

Metoclopramide may interact with the following drugs, supplyments, & may change the efficacy of drugs

Pregnancy Category Metoclopramide

Pregnancy

This medication should not be used during pregnancy unless the benefits outweigh the risks. If you become pregnant while taking this medication, contact your doctor immediately.

Lactation

This medication passes into breast milk. If you are a breast-feeding mother and are taking metoclopramide, it may affect your baby. Talk to your doctor about whether you should continue breast-feeding. Metoclopramide should not be used in children less than one year of age. It should only be used in children over one year of age when the benefits of treatment outweigh the risks of side effects. The total daily dose for children should not be higher than 0.5 mg per kilogram of body weight since with higher doses of tremors and abnormal twitching movements can occur.

References

  1. DrugBank
    Metoclopramide

    http://www.drugbank.ca/drugs/DB01233
    http://www.drugbank.ca/drugs/DB01233#enzymes
    http://www.drugbank.ca/drugs/DB01233#targets

  2. EPA DSStox

    https://comptox.epa.gov/dashboard/dsstoxdb/results?search=DTXSID6045169

  3. European Chemicals Agency (ECHA)

    https://echa.europa.eu/substance-information/-/substanceinfo/100.006.058

    https://echa.europa.eu/information-on-chemicals/cl-inventory-database/-/discli/details/27682

  4. Human Metabolome Database (HMDB)

    http://www.hmdb.ca/metabolites/HMDB0015363

  5. ClinicalTrials.gov

    https://clinicaltrials.gov/

  6. FDA Pharm Classes

    https://www.accessdata.fda.gov/spl/data/75a33c93-65d0-4f81-b7f7-709ec263c10e/75a33c93-65d0-4f81-b7f7-709ec263c10e.xml

    https://www.fda.gov/ForIndustry/DataStandards/StructuredProductLabeling/ucm162549.htm

  7. LiverTox

    https://livertox.nlm.nih.gov/Metoclopramide.htm

  8. NCIt

    https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C62046

  9. FDA/SPL Indexing Data

    https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystem-UniqueIngredientIdentifierUNII/

  10. EU Community Register of Medicinal Products

    https://ec.europa.eu/health/documents/community-register/html/ho25026.htm

  11. HSDB

    https://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+364-62-5

  12. FDA Medication Guides

    https://www.fda.gov/downloads/Drugs/DrugSafety/UCM176362.pdf

    https://www.fda.gov/downloads/Drugs/DrugSafety/UCM235574.pdf

  13. FDA Orange Book

    https://www.fda.gov/Drugs/InformationOnDrugs/ucm129662.htm

  14. MassBank of North America (MoNA)

    http://mona.fiehnlab.ucdavis.edu/spectra/browse?inchikey=TTWJBBZEZQICBI-UHFFFAOYSA-N

    http://www.nist.gov/srd/nist1a.cfm

  15. PubMed Health

    http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0001178/

    http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0011182/

    http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0011180/

  16. WHO ATC

    https://www.whocc.no/atc/

    https://www.whocc.no/atc_ddd_index/

  17. Wikipedia

    https://en.wikipedia.org/wiki/Metoclopramide

  18. PubChem

    https://pubchem.ncbi.nlm.nih.gov

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Cefquinome; Indications/Uses, Dosage, Side effects, Interaction ,Pregnancy

Cefquinome is a semisynthetic, broad-spectrum, fourth-generation aminothiazolyl cephalosporin with antibacterial activity. Cefquinome binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.

Mechanism of action of Cefquinome 

Cefquinome is a semisynthetic, broad-spectrum, fourth-generation aminothiazolyl cephalosporin with antibacterial activity. Cefquinome binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Respiratory diseases in horses caused by Streptococcus equi subsp. zooepidemicus and severe bacterial infections with a high risk of septicemia in foals in which Escherichia coli is involved.

Pharmacology of Cefquinome 

Cefquinome binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis. Respiratory diseases in horses caused by Streptococcus equi subsp. zooepidemicus and severe bacterial infections with a high risk of septicemia in foals in which Escherichia coli is involved.

………………………………………..Data or information not available

References

  1. EU Community Register of Medicinal Products

    https://ec.europa.eu/health/documents/community-register/html/vo2921.htm

    https://ec.europa.eu/health/documents/community-register/html/vo2422.htm

  2. European Chemicals Agency (ECHA)

    https://echa.europa.eu/information-on-chemicals/cl-inventory-database/-/discli/details/222498

  3. European Chemicals Agency – ECHA

    https://www.echa.europa.eu/web/guest/information-on-chemicals/cl-inventory-database/-/discli/details/222498

  4. FDA/SPL Indexing Data

    https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystem-UniqueIngredientIdentifierUNII/

  5. NCIt
    Cefquinome

    https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C79564

  6. Springer Nature
  7. Wikipedia

    https://en.wikipedia.org/wiki/Cefquinome

  8. PubChem

    https://pubchem.ncbi.nlm.nih.gov

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Cefpirome; Uses, Contra indications, Dosage, Side effects, Interaction

Cefpirome is a semisynthetic, broad-spectrum, fourth-generation cephalosporin with antibacterial activity. Cefpirome binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.

Cefpirome is a fourth-generation cephalosporin. Trade names include Cefrom, Keiten, Broach, Cefir. Cefpirome is considered highly active against Gram-negative bacteria, including Pseudomonas aeruginosa, and Gram-positive bacteria. It is marketed under the brand name of CEFROM by Sanofi Aventis group India.

Mechanism of action of Cefpirome

Cefpirome is a semisynthetic, broad-spectrum, fourth-generation cephalosporin with antibacterial activity. Cefpirome binds to and inactivates penicillin-binding proteins (PBPs) located on the inner membrane of the bacterial cell wall. PBPs are enzymes involved in the terminal stages of assembling the bacterial cell wall and in reshaping the cell wall during growth and division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity. This results in the weakening of the bacterial cell wall and causes cell lysis.

Dosage

Not available in the U.S.A

1-4 g IV q12hr

Renal Impairment

CrCl 20-50 mL/min: 1-2 g load, 0.5-1 g IV BID

CrCl 5-20 mL/min: 1-2 g load, 0.5-1 g IV qDay

CrCl <5 mL/min 0.25-0.5 g qDay

Other Information

Inject or infuse over 30 minutes

Other Indications & Uses of Cefpirome

Anaerobic cocci, Bacteroides spp., Enterobacter spp., E. coli, H. influenzae, Klebsiella spp., M. catarrhalis, M. morganii, Providencia rettgeri, Pseudomonas spp., Serratia spp., S. aureus, S. pneumoniae, S. pyogenes

Drug Interactions

Monitor Closely (14)

  • bazedoxifene/conjugated estrogens
  • conjugated estrogens
  • digoxin
  • estradiol
  • estrogens conjugated synthetic
  • estropipate
  • flucloxacillin
  • mestranol
  • mycophenolate
  • pivmecillinam
  • probenecid
  • sodium picosulfate/magnesium oxide/anhydrous citric acid
  • temocillin
  • ticarcillin

Minor (65)

  • aceclofenac
  • acemetacin
  • acyclovir
  • aminohippurate sodium
  • aspirin
  • aspirin rectal
  • aspirin/citric acid/sodium bicarbonate
  • aztreonam
  • balsalazide
  • bendroflumethiazide
  • biotin
  • bupropion
  • cefadroxil
  • cefamandole
  • cefdinir
  • ceftizoxime
  • celecoxib
  • chloramphenicol
  • chlorothiazide
  • chlorpropamide
  • chlorthalidone
  • choline magnesium trisalicylate
  • cyclopenthiazide
  • diclofenac
  • diflunisal
  • etodolac
  • etoricoxib
  • fenbufen
  • fenoprofen
  • flurbiprofen
  • furosemide
  • ganciclovir
  • hydrochlorothiazide
  • ibuprofen
  • indapamide
  • indomethacin
  • ketoprofen
  • ketorolac
  • ketorolac intranasal
  • lornoxicam
  • meclofenamate
  • mefenamic acid
  • meloxicam
  • mesalamine
  • methyclothiazide
  • metolazone
  • nabumetone
  • naproxen
  • niacin
  • oxaprozin
  • pantothenic acid
  • parecoxib
  • piroxicam
  • pyridoxine
  • pyridoxine (antidote)
  • rose hips
  • salicylates (non-asa)
  • salsalate
  • sulfasalazine
  • sulindac
  • thiamine
  • tolfenamic acid
  • tolmetin

………………………………….data or information not available

Reference

  1. ChemIDplus

    https://chem.nlm.nih.gov/chemidplus/sid/0084957299

    https://chem.sis.nlm.nih.gov/chemidplus/chemidheavy.jsp

  2. EPA DSStox

    https://comptox.epa.gov/dashboard/dsstoxdb/results?search=DTXSID2048244

  3. Human Metabolome Database (HMDB)

    http://www.hmdb.ca/metabolites/HMDB0041852

  4. FDA/SPL Indexing Data

    https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystem-UniqueIngredientIdentifierUNII/

  5. NCIt

    https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C79563

  6. WHO ATC

    https://www.whocc.no/atc/

    https://www.whocc.no/atc_ddd_index/

  7. Wikipedia

    https://www.wikidata.org/wiki/Q27274566

    https://en.wikipedia.org/wiki/Cefpirom

  8. PubChem

    https://pubchem.ncbi.nlm.nih.gov

  9. MeSH

    https://www.ncbi.nlm.nih.gov/mesh/67038950

    http://www.nlm.nih.gov/mesh/meshhome.html

    https://www.ncbi.nlm.nih.gov/mesh/6800090

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