Category Archive IH Diagnostic and Pain Management Hospital.

Specimen Collection

There are a variety of methods aimed at specimen collection to diagnose a UTI. Some of the factors that dictate the method used include patient comfort, the ability to void, and reducing the small risk of iatrogenic infection. Sterile collection methods can be employed, such as a suprapubic puncture or urethral catheterization, in an effort to reduce overdiagnosis and subsequent overtreatment.[rx] Even so, patients are instructed to collect their own samples from a variety of acceptable techniques.

Specimen Collection 

There are a variety of collection techniques for urine culture, including suprapubic aspiration, straight catheter technique, and mid-stream catch with or without cleansing. In pediatric patients who are not toilet trained, diaper collection, and sterile bag, urine collection methods are used. Suprapubic collection is the best method to avoid specimen contamination with bacteria, particularly in the distal urethra. Owing to patient discomfort, invasiveness, lack of indication (except in rare instances), and inappropriate resource use, this method is rarely deployed. Urine collection with a single catheter (straight catheter technique) is the next best option. Still, due to labor intensiveness as well as the possibility of introducing bacteria into the bladder, potentially causing a UTI, this technique is seldom used and only when indicated. The previously aforementioned methods of specimen collection are therefore reserved for those patients who are unable to self-collect. Hence, the most common method a urine sample is obtained for urine culture is via a clean-catch midstream technique, which is neither invasive nor uncomfortable. Colony counts from these samples correlate reasonably well compared to suprapubic aspiration and single catheter technique.[rx]

The current standards for self-collection include mid-stream clean-catch technique, mid-stream catch without prior cleansing, and random sampling delivered without instruction. There are no clinically significant differences seen between the various self-collection techniques.[rx] However, studies have shown that depending on the patient’s demographic, such as adult male, adult female, or infant/child, there may be preferred methods of sample collection over other methods. For females, contamination and diagnostic accuracy did not significantly change between midstream urine collection with or without prior cleansing; there is no recommendation without regard to cleansing prior to collection.[rx] In adult males, contamination was significantly decreased when mid-stream catch is utilized as the method of collection, becoming favorable over first-void specimen collection. Mid-stream collection was not significantly altered with prior cleansing. However, in children and infants, mid-stream collection with prior cleansing was favorable in reducing contamination over other methods, including mid-stream collection without cleansing, sterile bag urine collection, and diaper collection.[rx] Therefore, pre-collection cleansing procedures have been considered unnecessary in most adult populations as they do not decrease the risk of contamination from commensal bacteria.[rx][rx][rx] Even so, patients continue to follow the traditional directive of cleansing as the first step in urine specimen collection despite no change in diagnosis, course, or treatment.

Specimen Transportation

Owing to the probable increase risk of growth of colony-forming units (CFU) non-indicative of the patient’s true sample, urine specimens must be plated within two hours of collection, unless refrigerated or placed in a preservative.[rx] This measure decreases the risk of false-positive cultures, directly leading to a decrease in overtreatment while maintaining appropriate antibiotic stewardship.

Procedures

Specimen Preservation and Processing

Preservation of the urine sample can be achieved with a boric acid solution or refrigeration for up to 24 hours. Both techniques yield adequate preservation of the sample. Samples that are left at room temperature for greater than 4 hours run the risk of bacterial overgrowth of causative and contamination organisms.[rx] However, based on a meta-analysis of preservation techniques, the statistical analysis of this data was rated as low.[rx] Nonetheless, common gram-negative organisms causing UTIs such as Escherichia coli and Klebsiella pneumoniae, have been noted to be inhibited when boric acid is used as a storage medium. Therefore, careful consideration of the storage medium should be practiced, and timely refrigeration must be prioritized.

Specimens are processed routinely using calibrated loops for plating. This method allows for CFU/mL findings as well as the isolation of colonies for identification and susceptibility testing. Some of the most utilized media are blood agar and MacConkey agar. The temperature of the plates should be kept between 35 to 37 degrees Celcius with a recommended incubation time of 24 to 48 hours. However, Oligella urolytica, a slow-growing, gram-negative, and rare UTI-causing organism, has been reported to have an incubation of over 48 hours.[rx] Specimens from outpatients do not need to be plated on selective media. However, in hospitalized patients, where enterococci are the second leading cause of UTI, laboratory technicians should consider inoculating urine specimens to a medium that is selective for these gram-positive cocci.[rx]

Indications

Routine bacterial urine cultures are not always necessary in the evaluation of outpatients with uncomplicated UTIs and simple lower UTIs, such as uncomplicated cystitis.[rx][rx] An important classification of uncomplicated UTI versus complicated UTI distinguishes the need for urine culture. Since UTIs are composed of lower UTIs (e.g., cystitis) and upper UTIs (e.g., pyelonephritis), clinically differentiating the two by symptomology is necessary as the first step in determining the need for urine culture. A patient experiencing cystitis could report dysuria (with or without frequency), urgency, hematuria, or suprapubic pain, while a patient suffering from pyelonephritis may or may not have the symptoms of cystitis, but will typically report fever, chills, flank pain with or without costovertebral tenderness.[rx][rx] Should these patients have a complicating factor, a urine culture is likely warranted. Some of the complicating factors include male sex, chronic obstruction, chronic renal insufficiency, nephrolithiasis, poorly controlled diabetes, pregnancy, indwelling urinary catheters, indwelling urinary stent or nephrostomy tube, and immunosuppression (chronic high-dose corticosteroid use, use of other immunosuppressive agents, neutropenia, etc.).[rx] Furthermore, outpatients with recurrent UTIs, treatment failure, complicated UTIs, and inpatient UTIs require urine culture to not only document infection, but to confirm the causative organism in order to prevent complications and for antimicrobial susceptibility resistance. These examples warrant further investigation beyond clinical diagnosis and urinalysis.

Additionally, new-onset or worsening sepsis without evidence of an alternate source is also another appropriate indication for urine culture. New-onset or worsening sepsis is a major cause of morbidity and mortality in hospitalized patients globally and should be swiftly recognized clinically for the purposes of swift urine culture collection.[rx] Fever or alteration of consciousness without evidence of a source may also warrant a urine culture. For patients in early pregnancy or prior to certain urology procedures, screening for asymptomatic bacteriuria is warranted. Additionally, preoperative evaluations may trigger the utilization of urine culture, especially when mucosal bleeding is expected. Finally, urine cultures are sometimes appropriate in cases of spinal cord injury, where the patient may experience an increase in spasticity, autonomic dysreflexia, and a sense of unease.[rx] These patients are at an increased risk of UTI due to autonomic dysregulation leading to stagnating urine, which becomes a nidus for infection.

Urine culture is not indicated and is therefore deemed inappropriate when the urine characteristics are odorous, cloudy, or discolored in the absence of other localizing signs or symptoms, reflex urine cultures based on results of urinalysis such as pyuria in the absence of other indications, and to document successful response to therapy.[rx][rx] Screening for asymptomatic bacteria in most groups is also unnecessary, as it does not alter the course of therapy. Patients with asymptomatic bacteriuria are typically not treated unless pregnant. Yet, some studies have shown that in pregnant women with pyelonephritis, the patient course dictates antibiotic treatment, not necessarily the culture and sensitivities themselves.[rx]

Potential Diagnosis

The positive findings of a urine culture can lead to the diagnosis of UTI (uncomplicated vs. complicated), asymptomatic bacteriuria (ASB), catheter-associated UTI (CA-UTI), and catheter-associated asymptomatic bacteriuria (CA-ASB). These diagnoses lead to the possible identification of the source of sepsis. Proper diagnosis lends itself to proper antibiotic stewardship and decreases in morbidity and mortality. As up to 25% of hospitalized patients in North America receive indwelling catheter placement, utilization of the urine culture is of utmost importance to determine potential diagnoses.[rx][rx] Consequently, differentiation between catheterized patients and non-catheterized patients is common, as is the differentiation between UTI and asymptomatic bacteriuria.

Normal and Critical Findings

Normal Findings

Urine is normally sterile. However, there is a possibility of contamination. Hence, samples from patients without UTI symptoms with low colony counts certainly below the threshold for bacteriuria, and no detection of organisms, are considered to be normal samples.

Critical Findings

• UTI – UTI symptoms. Gold standard confirmation is the urine culture.[rx] Positive urine cultures are observed when there is significant microbial growth determined by standard microbiological criteria.[rx] Although not completely standardized, many laboratories set the cut-off at greater than or equal to 100,000 CFUs/ml for a UTI. However, this particular threshold may miss relevant infections. Consequently, other recommendations have noted a cut-off of greater than or equal to 1,000 CFUs/ml in order to capture other bacterial infections.[rx]
• CA-UTI – According to the Infectious Diseases Society of America’s (IDSA) 2010 guideline for diagnosis of CA-UTI, it is defined as patients with an indwelling catheter with the presence of symptoms or signs compatible with UTI with no other identified source of infection. They must also have greater than or equal to 1000 CFU/ml with more than one bacterial species in a single catheter urine specimen or in a midstream voided urine specimen in patients whose urinary catheter (urethral, suprapubic or condom) has been removed within the past 48 hours. According to the United States Centers for Disease Control and Prevention (CDC), the patient must meet the following three criteria: 1) The patient must have an indwelling urinary catheter in place for more than 2 days on the date of the event, 2) The patient has a fever (of greater than or equal to 38 degrees Celsius, costovertebral angle (CVA) pain or tenderness, suprapubic tenderness, urgency, frequency or dysuria, and 3) The patient has a urine culture with no more than two species of organisms identified, at least one being a bacterium of greater than or equal to 1000 CFU/ml.[rx]
• CA-ASB – Positive urine culture in the absence of UTI symptoms.[rx] Asymptomatic catheter-associated bacteriuria and candiduria exhibit a urine culture of at least 100,000,000 CFU/mL of an identified organism(s) in the absence of signs and symptoms of a UTI.[rx][rx] These cases do not require treatment and generally resolve upon the removal of catheters.[rx]
• Bacteriuria – The most commonly used cut-off for significant bacteriuria is greater than or equal to 100,000 CFU/ml of urine.[rx] Asymptomatic bacteriuria is present when the patient does not have any signs of a UTI clinically coupled with 100,000 CFU/ml exceeded in two consecutive samples of midstream urine (from women). For men, a single detection of more than 100,000 CFU/ml is adequate for diagnosis.[rx] Although pyuria is non-diagnostic in itself, the detection of leukocytes could support the diagnosis of CA-ASB.

The most common cause of UTIs in both inpatient and outpatient settings is Escherichia coli, accounting for the overwhelming majority of cases. E. coli is followed by coagulase-negative staphylococci, Klebsiella species, Proteus species, and Enterobacter species.[rx] Each unique organism can be part of urine culture results. Owing to the differences in the microbiology of each organism, proper identification leads to increased antibiotic stewardship by selecting the proper antibiotic coverage, subsequently leading to decreases in antibiotic resistance.

Interfering Factors

Urine culture results may be deemed faulty and inconclusive due to patient factors. Recent antibiotic use is a major culprit, as this therapy may mask the presence of UTI-causing organisms. Furthermore, the use of diuretics or the consumption of large amounts of fluids may also dilute the urine and invariably lead to a decrease in the number of bacteria present in the sample. Moreover, the large consumption of ascorbic acid has been long known to interfere with the results of urine dipstick results.[rx]

Culture results are invariably affected by faulty collection techniques, leading to the contamination of urine and invariably, by urogenital flora.[rx] Operator error in the handling of urine specimens may also lend to increasing CFUs, leading to false-positive results. Unless refrigerated or kept in a preservative, urine samples should be plated within two hours of collection.[rx] Urine samples where plating is delayed, especially over 24 hours, are deemed useless due to the possibility of a bacterial overgrowth that is not representative of the patient’s original sample. Consequently, laboratory delay is a significant issue interfering with the validity of the urine culture.

Complications

The various stages of urine collection, whether collection itself, storage, and preservation, have a tremendous impact on the results of a urine culture. Without adequate care, specimens can become contaminated with perineal, vaginal, or periurethral flora. The presence of the true pathogenic agent can be obscured due to the contamination, whether due to an overgrowth or an inhibition of the true pathogens. Even more than that, the medium in which the specimen is stored also plays a significant role in the true urinary pathogen. Inhibition of Escherichia coli and Klebsiella pneumoniae have been observed with the use of boric acid as the storage and preservation medium.[rx] Owing to these issues with contamination and obscuration of true UTI-causative organisms, misdiagnosis, and subsequent poor patient management and faulty antibiotic stewardship will result, with the most feared complication becoming a complicated UTI and possibly leading to urosepsis.[rx] Consequently, proper detection of UTI or asymptomatic bacteriuria is of paramount importance. For instance, swift detection of asymptomatic bacteriuria in pregnancy is necessary in order to prevent the feared complication of pyelonephritis with subsequent harm to the child.[rx] Ordering urine cultures when indicated and proper handling of the urine specimen provides for proper diagnosis and therefore preventing complications associated with poorly diagnosed and treated UTI.

Patient Safety and Education

Specimen collection by means of clean-catch midstream technique poses no risk to the patient. Despite the longstanding belief that pre-cleansing yields an uncontaminated specimen, several studies have shown that pre-cleansing has no significant effect on test results. Prevention of UTI is worthy of discussion and has been traditionally under-researched in the past. Patients should be educated on correct wiping methods, adequate hydration, frequent urination, avoiding feminine products, precoital bathing, and postcoital voiding, and avoid the use of a number of certain birth control products. With these increased measures aimed at improving hygiene, health behaviors, and sexual practices, UTI-related morbidity, and the use of antibiotics for these infections would invariably decrease.[rx][rx]

How is the test used?

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• https://medlineplus.gov/ency/article/003751.htm

Peritoneal dialysis is a way to remove waste products from your blood when your kidneys can’t adequately do the job any longer. This procedure filters the blood in a different way than does the more common blood-filtering procedure called hemodialysis.

During peritoneal dialysis, a cleansing fluid flows through a tube (catheter) into part of your abdomen. The lining of your abdomen (peritoneum) acts as a filter and removes waste products from your blood. After a set period of time, the fluid with the filtered waste products flows out of your abdomen and is discarded.

Peritoneal dialysis (PD) accounts for a small percentage (less than 7%) of the prevalent dialysis population in the United States compared to Canada (more than 50%). Better early survival on PD compared to hemodialysis (HD) has also been reported by several observational studies, including national registries from different parts of the world.  The cost of HD per patient per year remains significantly higher than for PD ($87,945 for HD versus $71,630 for PD in 2011). Patients have a choice when initiating dialysis to use HD or PD. Choice should be patient-centered and made after careful considerations of all factors that may alter outcomes. A large US cohort study of over 6000 matched pairs of dialysis patients beginning dialysis in 2003, showed that 1-year patient survival was significantly higher for PD when compared to HD (85.8% versus 80.7% (p < 0.01)). However, 80% of end-stage renal disease (ESRD) patients in the United States start hemodialysis (HD) with a tunneled hemodialysis catheter (TDC), and 60% continue to dialyze using an HDC for 91 days after dialysis initiation.  This initial catheter (modality) choice has had a major impact on the mortality of ESRD patients. Patient mortality in the first 90 days of HD as a result of catheter-associated bacteremia and sepsis from TDC use is higher when compared to patients initiating dialysis on PD.  A significant percentage of deaths in HD occurred within the first the 90 days on dialysis.[rx][rx]

Indications

Medicine is moving to quality-driven models; every clinician needs to weigh the risk of early use TDC to start HD compared to the benefit of starting peritoneal dialysis using a peritoneal dialysis catheter (PDC).

Contraindications

PD is contraindicated in patients with:

• Uncorrected abdominal wall hernia
• Pleuroperitoneal shunt
• Abdominal adhesions

Equipment

PD Catheter Placement[rx][rz]

Utilizing several different techniques, the success rate of PDC placement reported in the literature varied from 80% to 100%. Are there any differences in catheter outcomes based on the technique used to place PDC? The answer to this question is difficult, as there are wide variations in inpatient and operator factors that cannot be controlled across populations. Overall, open surgical placement was associated with the highest number of complications, including poor function, leaks, and catheter migrations; there was a trend toward higher catheter survival after laparoscopic insertion. (See Table 1) Randomized control trial comparing fluoroscopic versus laparoscopic PDC placement included 113 patients showed a complication-free catheter survival that was significantly higher at 42.5% (95% CI 29.3 – 55.0) in the percutaneous group compared with 18.1% (95% CI 8.9 – 29.8) in the laparoscopic group (p = 0.03). One-year patient and catheter survival in the 2 groups was no different.

Both surgical and percutaneous procedures have low complication rates when performed by experienced operators. Obese patients who have had previous abdominal surgery or with previous episodes of PD-related peritonitis can benefit from the advanced laparoscopic placement of the catheter. Surgical PD catheter implantation typically takes longer, including referral and consultation delays to a surgeon, operating room scheduling, and preoperative medical and anesthesia clearance. In contrast, nephrology-guided PD catheter placement can be performed relatively quickly, usually under procedure sedation analgesia in an outpatient setting. This is particularly useful in an acute emergent setting with a relatively short window of notice required before dialysis initiation.

Preparation

Peritoneal Dialysis Benefit

Starting dialysis with a PDC is preferable to an HDC in terms of patient morbidity, mortality, and cost. It has also been shown in large observational retrospective studies that there is a survival advantage for PD over HD in the first 1 to 3 years of dialysis. The 2013 Annual Data Report from the United States Renal Data System also shows a significantly improved adjusted probability of 5-year survival with PD compared to HD. This early survival, for the most part, may be explained by selection bias because healthier patients may be more likely to choose PD as their modality. Patients with comorbid conditions tend to start HD after an acute illness and have high early mortality that is wrongly attributed to their HD modality.

Two recent studies from Canada tried to address the selection bias in PD outcomes. Quinn et al. studied 6573 patients who had at least 4 months of follow-up with nephrologists and had an elective outpatient start of dialysis. There was no difference in 2-year mortality between PD and HD, and in patients without diabetes, PD was associated with a survival benefit that extended beyond 2 years of follow-up. Similarly, Perl et al., comparing incident ESRD patients from a cohort of 40,000 patients in Canada, noted an 80% increased risk of death in patients starting HD using a central venous catheter (CVC) but no difference in mortality between PD and HD using AVF or arteriovenous graft (AVG) for dialysis.[rx]

Technique

Peritoneal dialysis is one of the modalities utilized for dialysis. There are several advantages of PD versus HD. Patients using PD will not need to leave home every other day to get dialysis, rather they perform their treatments at home using a very simple principle for removing toxins from their body.

Patients selected for PD will undergo PD catheter placement using one of the several techniques described above. Once the catheter has healed, they undergo technique training at a dialysis unit for 2 to 3 weeks, learning the proper aseptic technique to use the catheter for dialysis. The basis of toxin removal in PD is diffusion of uremic toxins out of the blood through the peritoneal membrane into the peritoneal fluid, that is then discarded after a specified amount of time in the peritoneal cavity.[rx]

The process of PD can be automated using a simple machine attached to peritoneal dialysis fluid bags. The machine is programmed to infuse the predetermined volume of fluid into the peritoneal cavity, dwell fluid in the peritoneal cavity for a specified time, and automatically drain the fluid. Cycles are repeated several times based on patients needs and peritoneal membrane diffusion characteristics. Manual exchanges require the installation and draining of fluid to be performed by the patient, repeating the process several times during the day to achieve the required clearance of toxins.

Complications

Infection of the peritoneal cavity is the most important complication that will not only increase the risk of PD failure but also potentially be life-threatening to the patient. The rate of PD infections can be lowered by proper technique and constant patient education to emphasize proper aseptic technique while using the PDC. Most infections will present with abdominal pain and cloudy peritoneal fluid and are diagnosed by looking for white blood cells (WBCs) in the PD fluid. A cell count of more than 100 WBCs per mL of the fluid suggests infection and should be promptly addressed per guidelines.[rx]

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ECG is a non-invasive diagnostic modality that has a substantial clinical impact on investigating the severity of cardiovascular diseases.[rx] ECG is increasingly being used for monitoring of patients on antiarrhythmics and other drugs, as an integral part of preoperative assessment of patients undergoing non-cardiac surgery, and for screening individuals in high-risk occupations and those who are participating in sports. Also, EKG serves as a research tool for surveillance and experimental trials of drugs with recognized cardiac effects.[rx] Cardiovascular disease, as the number one cause of death, puts a great emphasis on healthcare providers to develop skills and knowledge in interpreting ECGs to provide the best care promptly. Many healthcare providers find the advanced interpretation of ECG findings a complicated task. Errors in the analysis can lead to misdiagnosis resulting in delaying the appropriate treatment. This activity seeks to provide a general understanding of the ECG mechanisms, interpretation techniques, and commonly encountered ECG findings.

Anatomy and Physiology

A basic understanding of cardiac anatomy and coronary distribution is essential to understand the electrocardiographic findings.

The heart is a vital organ of the body and occupies the space in the central chest between the lungs. Together with the blood vessels and blood, it constitutes the circulatory system of the body. The heart is a muscular organ comprised of four chambers that includes two atria (right and left) opening into right and left ventricles via tricuspid and mitral valves, respectively. A wall of muscle called the septum separates all four chambers. The heart receives deoxygenated blood from the whole body via superior and inferior vena cava, which first enters the right atrium. From here, it transits through the right ventricle and then passes into the lungs via the right and left pulmonary arteries, where it is oxygenated. The oxygenated blood from the lungs pours into the left atrium through the right and left pulmonary veins, and from here, it is pumped by the left ventricle into the aorta to the rest of the body. The heart derives its blood supply from the coronary arteries that branch off from the aorta. The right and left coronary arteries lie on the surface of the heart. With considerable heterogeneity among the general population, different regions of the heart receive vascular supply by the various branches of the coronary arteries. This anatomic distribution is significant because these cardiac regions are assessed by a 12-lead ECG to help localize and diagnose ischemic or infarcted areas. Written below are the following regions supplied by the different coronary arteries.

• Inferior Wall – Right coronary artery
• Anteroseptal – Left anterior descending artery
• Anteroapical – Left anterior descending artery (Distal)
• Anterolateral – Circumflex artery
• Posterior Wall – Right coronary artery

The heart is a mechanical pump whose activity is governed by the electrical conduction system. It is essential to have a good understanding of the physiology of the cardiac cells as this will help the reader appreciate how the heart works and the implications of findings on the ECG. The heart is made up of specialized cardiac muscle, which is striated and organized into sarcomeres. These muscle fibers contain a single central nucleus, numerous mitochondria, and myoglobin molecules. Extensive branching of the cardiac muscle fibers and their end-to-end connection with each other through intercalated discs make them contract in a wave-like fashion. This mechanical work of pumping blood to the whole body occurs in a synchronized manner and is under the control of the cardiac conduction system. It is comprised of two types of cells, pacemaker and non-pacemaker cells. Pacemaker cells are located primarily in the SA and AV node, and it is the SA node, which drives the rate and rhythm of the heart. The AV node gets suppressed by the more rapid pace of the SA node. [rx] The specialized function associated with the pacemaker cells is their spontaneous depolarization with no true resting potential. When spontaneous depolarization reaches the threshold voltage, it triggers a rapid depolarization followed by repolarization. The non-pacemaker cells mainly comprise the atrial and ventricular cardiac muscle cells and Purkinje fibers of the conduction system. They consist of true resting membrane potential, and upon initiation of an action potential, rapid depolarization is triggered, followed by a plateau phase and subsequent repolarization. Action potentials are generated by ion conductance via the opening and closing of the ion channels. Knowing which ECG leads corresponds to specific arteries helps in localizing the obstruction in acute ST-elevation MI or an age-indeterminate Q-wave infarction by observing predictable patterns on the ECG.[rx]

Indications of Electrocardiogram

The evolution of EKG from a string galvanometer to the modern-day advanced computerized machine has led to its use as a diagnostic and screening tool, making it the gold standard for diagnosing various cardiac diseases.

Owing to its widespread use in the field of medicine, the EKG has several indications listed below:

• Symptoms are the foremost indication in use for the EKG which includes palpitation, dizziness, cyanosis, chest pain, syncope, seizure, and poisoning
• Symptoms or signs associated with heart disease including tachycardia, bradycardia and clinical conditions including hypothermia, murmur, shock, hypotension, and hypertension
• To detect myocardial injury, ischemia, and the presence of prior infarction as well
• Rheumatic heart disease[rx]
• EKG changes in cases like drowning and electrocution are very valuable in the determination of necessary interventions[rx]
• Detecting pacemaker or defibrillator device malfunction, evaluate their programming and function, verify the analysis of arrhythmias and monitor for delivery of the appropriate electrical pacing in patients with defibrillators and pacemakers[rx]
• Evaluation of metabolic disorders
• Helpful for the assessment of blunt cardiac trauma[rx]
• Cardiopulmonary resuscitation
• Valuable aid in the study and differential diagnosis of congenital heart diseases[rx]
• Electrolyte imbalance and rhythm disorders[rx]
• To monitor the pharmacotherapeutic effects and adverse effects of drug therapy
• Perioperative anesthesia monitoring including preoperative assessment and intraoperative and postoperative monitoring
• Screening tool in a sports physical exam to rule out cardiomyopathy[rx]

Contraindications of Electrocardiogram

There are no absolute contraindications for EKG. The relative contraindications to its use include:

• Patient refusal
• Allergy to the adhesive used to affix the leads

Equipment

The American College of Cardiology (ACC), in conjunction with American Heart Association (AHA) and the Heart Rhythm Society (HRS), has formulated guidelines and also set technical standards for ECG equipment [rx]. With advancements, most of the EKG machines are digital and can autogenerate preliminary findings based on the morphology criteria.

The conventional ECG machine consists of 12 leads, which divide into two groups, i.e., limb leads and precordial leads. Limb leads are further categorized as standard bipolar limb leads I, II, and III, and augmented unipolar leads aVL, aVF, and aVR. The precordial leads include V1 to V6. The limb leads view the heart in a vertical plane, and the precordial leads record the electrical activity of the heart in the horizontal plane. The ECG represents a graphic recording of the electrical cardiac activity tracing on the electrocardiograph paper. The fundamental principle behind the recording of an ECG is an electromagnetic force, current, or vector that has both magnitude and direction. When a current of depolarization travels towards the electrode, it gets recorded as a positive deflection, and when it moves away from the electrode, it appears as a negative deflection.

• A current of repolarization traveling away from the positive electrode is seen as a positive deflection and towards a positive electrode as a negative deflection
• When the current is perpendicular to the electrode, it touches the baseline and produces a biphasic wave.

These concepts are easily applied to the heart while recording the ECG. There are several types of ECG monitoring equipment available, including continuous ECG monitoring, hardwire cardiac monitoring, telemetry, ambulatory electrocardiography, transtelephonic monitoring, and wireless mobile cardiac monitoring systems, etc. Furthermore, a duo of ECG and electronic stethoscopes have been designed into a portable, handheld device that can review ECG rhythms and intervals at the bedside for analysis. With the evolution of technology, there are electronic wristwatches that can also provide monitoring of the heart rate and rhythm and have proven to be of value in detecting atrial fibrillation.[rx] The accuracy of these devices, however, may be somewhat inferior when compared to a 12-lead ECG; and when prompted for abnormal findings, these require confirmation by standardized clinical testing available in the Cardiology office.

The equipment for performing a conventional 12-lead ECG includes:

• Electrodes (sensors)
• Gauze and skin preparation (alcohol rub) solution
• Razors or clippers or a roll of tape (for hair removal)
• Skin adhesive and/or antiperspirant
• ECG paper
• Cardiac monitor or electrocardiography machine

Personnel

The medical personnel that can perform the ECG procedure includes a doctor, nurse, or a qualified technician. Usually, it is performed by the technicians either in the clinics or hospitals and then interpreted by physicians. Often, these findings are confirmed by a cardiologist in a hospital-based setting.

Preparation

ECG merely requires special preparation. Before the procedure, a brief history regarding drugs and allergy to adhesive gel is necessary. The temperature of the room must be kept optimal to avoid shivering. The patient should be in a gown, and electrode sites identified. For good contact between the body surface and electrodes, it is advised to shave the chest hair and then apply the electrocardiographic adhesive gel for electrodes. Any metallic object like jewelry or a watch requires removal, if possible. Limb and precordial leads should be accurately placed to avoid vector misinterpretation. The patient must lie down and relax before recording the standard 10-second strip.

Technique

ECG machines are designed to record changes in electrical activity by drawing a trace on a moving electrocardiograph paper. The electrocardiograph moves at a speed of 25mm/sec. Time is plotted on the x-axis and voltage on the y-axis. In the x-axis, 1 second is divided into five large squares, each of which represents 0.2 sec. Each large square is further divided into five small squares of 0.04 sec each. The EKG machine is calibrated in such a way that an increase of voltage by one volt should move the stylus by 1 cm. The conventional 12-lead EKG consisting of six limbs and six precordial leads is organized into ten wires. The limb leads include I, II, III, aVL, aVR, and aVF and named as RA, LA, RL, and LL. The limb leads are color-coded to avoid misplacement (red- right arm, yellow- left arm, green- left leg, and black- right leg). The precordial leads V1 to V6 are attached to the surface of the chest.[rx]  For the correct location, the “Angle of Louis” method is an option, and the exact placement is as follows:

• V1 is placed to the right of the sternal border, and V2 is situated at the left of the sternal edge.
• V4 is placed at the level of the fifth intercostal space in the mid-clavicular line. V4 should be placed before V3. V3 is placed between V2 and V4.
• V5 is placed directly between V4 and V6.
• V6 is placed at the level of the fifth intercostal space in the mid-axillary line.
• V4 through V6 should line up horizontally along with the fifth intercostal space.

Complications

ECG is a safe, non-invasive, painless test with no major risks or complications. An allergic reaction or skin sensitivity to the adhesive gel can occur and usually resolves as soon as the electrode patches are removed, and in most cases, do not require any treatment. Artifacts and distortions pose serious diagnostic difficulties and may result in an inaccurate interpretation of the ECGs that may potentially result in an adverse therapeutic intervention.[rx][rx]

There can be a potential for misdiagnosis due to the inadvertent misplacement of ECG leads.[rx][tx]

Clinical Significance

Evaluation of Arrhythmia

In patients suspected of arrhythmias, an electrocardiogram (EKG) is the first step and will usually give the diagnosis. However, at times, the patient may suffer from paroxysmal arrhythmia. The following modalities can be used for diagnosing based on the frequency of the symptoms a patient has secondary to a suspected arrhythmia.

• Ambulatory EKG monitoring for patients with frequent symptoms
• The event recorder needs to be triggered by the patient to record and will not a viable choice for patients with syncope.
• Loop event recorder records up to 2 minutes before the trigger. It is good for patients with syncope.
• Implantable loop recorder for patients with less frequent symptoms.

Tachyarrhythmia

Tachyarrhythmia is defined as an abnormal rhythm with a ventricular heart rate of 100 beats per minute or more. It can be further classified based on the origin of the arrhythmia into:

Supraventricular Tachycardia (SVT): Arrhythmia originating from above the AV node (from atrial origin or AV junction origin).

• Atrial fibrillation (AFib)
• Atrial flutter
• Atrial tachycardia
• Atrial premature complex (PAC)
• Atrioventricular nodal reentrant tachycardia (AVNRT)
• Atrioventricular reentrant tachycardia (AVRT)
• AV junctional extrasystoles

Ventricular Tachycardia (VT): The origin of the arrhythmia is below the AV node.

• Ventricular fibrillation (V-fib)
• Ventricular premature beats (PVC)
• Ventricular tachycardia (sustained or non-sustained)

Tachyarrhythmias can also be classified based on the QRS complex duration into

Narrow QRS complex tachycardia when QRS is <120 milliseconds in duration:

• Sinus tachycardia
• Atrial tachycardia (AT)
• Atrial flutter
• Atrioventricular nodal reentrant tachycardia (AVNRT)
• Atrioventricular reentrant tachycardia (AVRT)
• Junctional ectopic tachycardia
• Sinoatrial nodal reentrant tachycardia (SANRT)
• Atrial fibrillation (irregular QRS complexes)

Wide QRS complex tachycardia (QRS ≥120 milliseconds in duration) is classified as monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, or ventricular fibrillation.

Supraventricular Tachycardia Syndromes

• These are usually narrow complex tachycardias with QRS width being less than 3 mm or 120 milliseconds on the EKG strip. Supraventricular tachycardia is further classified into atrioventricular reciprocating tachycardia, atrioventricular nodal reentrant tachycardia, and atrial tachycardia based on the mechanism of tachycardia. [rx][rx]

I. Atrioventricular reciprocating tachycardia (AVRT)

As found in Wolff-Parkinson-White syndrome (the presence of delta wave without arrhythmia doesn’t require investigation or treatment).

• Mechanism: Accessory pathway present outside of the AV node-Bundle of Kent. It can be further categorized into:
• • Antidromic: Conduction down the accessory pathway and up to AV node leading to the formation of a delta wave.
  • Orthodromic: Conduction down the AV node into an accessory pathway with no delta wave.
• Signs & Symptoms: Palpitation, shortness of breath, or syncope.
• EKG Findings: Slurred upstroke of the QRS, delta wave, may give an impression of the wide QRS complex.
• Management: Amiodarone or procainamide. If this fails, the next step is synchronized cardioversion.
• Definitive Therapy: Ablation of the accessory pathway.

 II. Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

• Mechanism: Slow & fast fibers present in AV node & peri-nodal tissue leading to re-entry. Signs & Symptoms: Sudden tachycardia, palpitation, shortness of breath, chest tightness, or syncope. EKG Findings: Narrow complex tachycardia with P waves hidden in T waves. Heart rate is in the range of 150-160 bpm.

Management

• Step 1: Carotid massage/Valsalva maneuver
• Step 2: Adenosine
• Step 3: Cardioversion
• Step 4: Ablation or chronic suppressive therapy with beta-blockers and calcium channel blockers such as diltiazem/verapamil.

 III. Atrial fibrillation

It is the most common arrhythmia in the United States. It affects more than 20% of the general population at some time in their lives.[rx] There are five types based on their duration:[rx]

• • New-onset]
  • Paroxysmal: Self-terminating or intermittent
  • Persistent: Fails to self-terminate within 7 days and requires treatments (medical or electrical cardioversion)
  • Long-standing Persistent: Lasts for ≥ 1 year
  • Permanent: Persistent for ≥ 1 year despite treatment
• Mechanism: Multiple reentrant wavelets due to atrial ectopy from muscle fibers near the proximal part of the pulmonary vein.
• Signs & Symptoms: It can be asymptomatic or can cause symptoms like palpitation, shortness of breath, irregularly irregular pulse, or even hypotension.
• EKG Findings: Irregularly irregular narrow complex tachycardia with no discernable P-waves.
• Management: The management strategy for atrial fibrillation can be classified into rate control or rhythm control. The decision to use a rate control or a rhythm-control strategy depends on the hemodynamic stability, candidacy for ablation, and the presence of co-morbidities. Patients with atrial fibrillation are at increased risk of ischemic-embolic stroke, and anticoagulation recommendations are based on the CHA2DS2VaSc score.
• CHA2DS2VaSc score is determined by the presence of the following factors: Congestive heart failure (CHF) with ejection fraction (EF) less than 40%, hypertension, age > 65 years, diabetes mellitus, history of stroke (non-hemorrhagic) or transient ischemic attack (TIA), vascular disease (peripheral vascular disease – PVD), age > 75 years, female sex. Each factor adds a point to the score, except for a history of stroke/TIA, which adds 2 points.

• • If the score is 0: No anticoagulation or aspirin based on individual assessment
  • If the score is 1: Aspirin or anticoagulation based on individual assessment.
  • If the score is 2 or more: Anticoagulation is recommended if not at high risk of bleeding.
• Rate Control Strategy: The heart rate goal is < 110 bpm in patients with chronic atrial fibrillation. It can be achieved with either beta-blockers or calcium channel blockers. Digoxin is usually used as adjuvant therapy in a patient with difficulty controlling rate or in heart failure patients.
• Cardioversion Strategy: Cardioversion is preferred in hemodynamically unstable patients or if rate control fails. It is also preferred in a young patient with no other co-morbidities. Cardioversion can be performed within 36 hrs of the onset of atrial fibrillation, but if the presentation is delayed or is of unknown duration, the absence of thrombi needs to be confirmed with a transesophageal echocardiogram (TEE). If a thrombus is present on an echocardiogram, the patient will need anticoagulation for at least three weeks before cardioversion can be performed. The patient needs to be on anticoagulation for at least four weeks post cardioversion. Various modalities are available for cardioversion therapy and include synchronized electric cardioversion or chemical cardioversion with medications including flecainide, propafenone, amiodarone, or dronedarone. Maze procedure is usually reserved for the patient undergoing other cardiac surgery.

Atrial Flutter

• Mechanism: Reentrant circuit usually around the tricuspid annulus in the right atrium.[rx]
• Signs & Symptoms: Can be asymptomatic, or it can cause palpitation, shortness of breath, or hypotension.
• EKG Findings: Regular tachycardia with Saw-tooth appearance of P wave with a variable degree of AV block.
• Management: General goals include control of ventricular rate with AV blocking agents (beta-blockers or calcium channel blockers), but the restoration of sinus rhythm through cardioversion or ablation is preferred.

Multifocal Atrial Tachycardia (MAT)

• Mechanism: multiple automatic atrial foci due to increased sympathetic tone secondary to various causes, including hypoxemia (chronic obstructive pulmonary disease (COPD), or stimulant use.
• Signs & Symptoms: Usually asymptomatic. Patients will have symptoms of the underlying illness, such as dyspnea.
• EKG Findings: Three or more P wave morphologies with different PR intervals.
• Management: Oxygen therapy if hypoxemic and treatment of the underlying cause.
• Refractory cases: Rate Control with calcium channel blockers as the first choice in the setting of COPD followed by beta-blockers.

Junctional tachycardia

• Mechanism: Rhythm arising from the AV node.
• Risk Factors: Post cardiac surgery, myocardial ischemia (or during reperfusion), or digoxin toxicity.
• Signs & Symptoms: Usually well-tolerated and asymptomatic.[rx]
• EKG Findings: Inverted P Wave in the lead 2 with short PR or No P waves with a narrow complex.
• Management: Treat the underlying cause.

 IV. Ventricular Tachycardia

Origin is below the AV node. It is the major cause of sudden cardiac deaths in the United States.

a) Non-Sustained Ventricular Tachycardia:[rx] When the rapid ventricular rhythm terminates on its own within 30 seconds.

• Mechanism: Channelopathies secondary to structural abnormality, electrolyte disturbances, metabolic imbalance, and the effect of pro-arrhythmic drugs.
• Risk Factors: Structural or ischemic heart disease.
• Signs & Symptoms: Asymptomatic or palpitations.
• EKG Findings: Monomorphic wide complex with more than three beats in a row but lasts less than three seconds.
• Management: Implantable cardioverter-defibrillator (ICD) and/or medical therapy.

b) Sustained Ventricular Tachycardia

• Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current. Some patients do not have structural heart disease. Approximately 10% of the cases are idiopathic.
• Risk Factors: Structural heart disease and post-myocardial infarction.
• Signs & Symptoms: Palpitation, hypotension, or syncope.
• EKG Findings: Monomorphic wide complex tachycardia.
• Management: Intravenous lidocaine, amiodarone, or procainamide. Catheter ablation is an option too.

c) Ventricular Fibrillation

• Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current leading to disorganized high-frequency excitation. Patients with Cardiomyopathies can have Ventricular fibrillation due to an increase in end-diastolic pressure, wall tension, or the presence of abnormal channels in ventricular fibers.
• Risk Factors: Structural heart disease and post-myocardial infarction.
• Signs & Symptoms: Syncope and death if not treated immediately.
• EKG Findings: Polymorphic fibrillatory waves.
• Management: Unsynchronized cardioversion followed by amiodarone.

d) Torsades De Pointes

• Mechanism: It is usually precipitated by premature ventricular contraction leading to “R on T phenomenon.”
• Risk Factors: Congenital long QTc with hypokalemia and hypomagnesemia.
• Signs & Symptoms: Syncope and death if not treated immediately.
• EKG Findings: Polymorphic wide-complex tachycardia with a heart rate > 300 bpm.
• Management: Intravenous magnesium or Isoproterenol, which increases heart rate and decreases QT-duration. Avoid hypokalemia and hypomagnesemia. Chronic therapy with beta-blockers in patients with long QT syndrome.

3. Bradyarrhythmias

Bradyarrhythmia is defined as a heart rate below 60 beats per minute (bpm) and comprises several rhythm disorders, including atrioventricular (A-V) blocks and sinus node disorders.[rx][rx]

Sinus Bradycardia

• Mechanism: Increased vagal tone. It can be physiological in athletes.
• Signs & Symptoms: Usually asymptomatic. It can lead to orthostasis or dizziness if pathological.
• EKG Findings: Sinus rhythm with an upright P wave in lead II and biphasic in V1.
• Management: No treatment is required unless pathological with an inadequate heart rate increase with leg raise test. Treat with isoproterenol or pacemaker if no relief.

Atrioventricular Blocks

• Mechanism: Atrial impulses are conducted with a delay or not at all when an electrical impulse reaches a tissue that not excitable or is in a refractory period.

a) First Degree AV Block: Caused by increased vagal tone or conduction impairment or due to medications.

• Signs & Symptoms: Generally asymptomatic but can cause dizziness.
• EKG Findings: PR interval is greater than 200 milliseconds.
• Management: Usually, no need to treat.

 b) Second Degree AV Block: Further classified into Mobitz I block, where there is a progressive prolongation of the PR interval followed by a skipped beat, and Mobitz II block, where there is a randomly dropped QRS complex on an EKG.

• Sign & Symptoms: Can be asymptomatic, dizziness, palpitations, weakness, syncope.
• EKG Findings: Mobitz type I shows progressive prolongation of the PR interval followed by a dropped QRS complex or dropped beat. Mobitz type II has randomly dropped QRS complexes.
• Management: Pacemaker is indicated in symptomatic Mobitz I and all of Mobitz II heart block.

c) Third Degree or complete AV Block

• Mechanism: Lack of conduction of atrial impulse to ventricle leading to independent contractions.
• Sign & Symptoms: Profound bradycardia, hypotension, and can lead to asystole and cardiac arrest.
• EKG Findings: Bradycardia, P waves occur independently of QRS and Wide QRS for ventricular rhythm.
• Management: Pacemaker placement.

Sinus Node Dysfunction

• Mechanism: Senescence of the SA node, an ischemic event involving SA node leading to impulse generation at a slower rate.

a) Sinus Pause: When the SA node has delayed impulse generation.

b) Sinus Arrest: Failure of impulse generation.

c) SA Nodal Exit Block: Failure of impulse transmission.

• Sign & Symptoms: Bradycardia, dizziness, palpitation, or syncope.
• EKG Findings: P wave not originating at a determined rate with regularity
• Management: Symptomatic patients require pacemaker placement.

The goal of the ECG interpretation is the ability to determine whether the ECG waves and intervals are normal or pathological. Electrical signal interpretation gives a good approximation of heart pathology. A standard 12 lead ECG is shown in. The best way to interpret an ECG is to read it systematically:

• RATE: For calculation of rate, the number of either small or large squares between an R-R interval should be first calculated. The rate can be calculated by either dividing 300 by the number of big squares or 1500 by the number of small squares between two R-waves. For an irregular rhythm, count the number of beats in a 10-second strip and multiply it by 6.[rx] Normal HR is 60 to 99 beats per minute. If it is less than 60, it’s called bradycardia and if greater than 100/min, it’s called tachycardia
• RHYTHM: The leads I, II, aVF, and V1 require inspection for an accurate interpretation of rhythm. It involves looking for five points: the presence or absence of regular P waves, duration of QRS complexes (narrow or wide), the correlation between P waves and QRS complexes, whether the rhythm is regular or irregular, and also importantly, the morphology of P-waves. A regular rhythm ECG has regular P waves, each preceding a QRS complex in a regular rhythm. Also, normal sinus rhythm demonstrates positive P-waves in leads I, II, and aVF, suggesting a downward propagation of atrial activation from the SA node. These features also help in identifying if the arrhythmia is originating in the atria or ventricles.[rx] Many disorders are related to rhythm abnormalities. For example, in atrial fibrillation, no real P waves can be seen due to the very fast atrial activity, and only a few impulses get delivered to ventricles making the rhythm irregularly irregular. The presence of ‘irregularly irregular’ narrow QRS complexes with no discrete P waves is the hallmark feature in the identification of atrial fibrillation.
• CARDIAC AXIS: It refers to the general direction of the heart’s depolarization wavefront in the frontal plane. The cardiac axis is related to the area of significant muscle bulk within the healthy conducting system. A typical cardiac axis is between -30 to +90 degrees. A quick way to estimate the axis is by looking at leads I and aVF. It can be defined as a normal axis when the QRS complex is positive in both leads I and aVF. A left axis deviation (between 0 and -90 degrees) is defined by the presence of positive QRS in the lead I and negative in lead aVF and right axis deviation(+90 and 180 degrees) by the presence of QRS negative in the lead I and positive in lead aVF. If both QRS complexes are negative in leads I and aVF, it is termed as extreme right axis deviation or indeterminate axis (-90 to 180 degrees).[rx] Other methods used for the determination of the cardiac axis include three lead analysis, isoelectric lead analysis, etc. There are several disorders in which the cardiac axis deviates.  Examples include conditions like old inferior MI, left ventricular hypertrophy, left bundle branch block where left axis deviation occurs while noting right axis deviation in conditions including right ventricular hypertrophy, pulmonary hypertension, hyperkalemia, and wolf-Parkinson-White syndrome, etc. The specific criteria on ECG for atrial and ventricular hypertrophy are devised from examining various leads and wave morphologies: for atrial abnormality (enlargement/ hypertrophy), leads II and V1 are usually assessed. Right atrial hypertrophy shows an increase in the amplitude in the first half of the P waves by 2.5 mm in inferior leads and a possible right axis deviation.[rx] It is often termed as P pulmonale because of its frequent association with chronic obstructive lung disease. Left atrial hypertrophy shows an increase in the amplitude of the terminal component and duration of the P wave, and it must descend at least 1 mm below the isoelectric line in lead V1 and must be at least 0.04 seconds (40 ms) in width. As the left atrium is electrically dominant, it shows no axis deviation.[rx]For the diagnosis of ventricular hypertrophy, it requires looking at several leads on the ECG. The right ventricular hypertrophy characteristically shows by right axis deviation along with the presence of a more significant R wave than S wave in lead V1, whereas in lead V6, a more significant S wave than R wave.[rx] Left ventricular hypertrophy is characterized by voltage criteria either by calculating the voltage of  R wave in V5 or V6 plus the S wave in V1 or V2 exceeding 35mm or by the voltage of R wave exceeding 13 mm in lead aVL. Infrequently, there is also the presence of secondary repolarization abnormalities, including asymmetric T wave inversion and downsloping  ST-segment depression, commonly also referred to as the strain pattern; the left axis deviation often accompanies this.[rx]
• P-WAVE: It represents atrial depolarization on the ECG. As atrial depolarization initiates by the SA node located in the right atrium, the right atrium gets depolarized first, followed by left atrial depolarization. So the first half of the P-wave represents right atrial depolarization and the second half left atrial depolarization. Its duration is three small squares wide and 2.5 small squares high. It is always positive in the lead I and II, and consistently negative in lead aVR in normal sinus rhythm. It is commonly biphasic in lead V1. An abnormal P-wave may indicate atrial enlargement.[rx]
• PR INTERVAL: It represents the time from the beginning of atrial depolarization to the start of ventricular depolarization and includes the delay that occurs at the AV node. The average interval is 3 to 5 small squares (120 to 200ms).[rx] Variations in the PR interval can lead to various disorders. Long PR interval may indicate first-degree AV block, and short interval may be present in conditions with accelerated AV conduction such as the presence of bypass tract or Wolf-Parkinson-White syndrome and Lown-Ganong-Levine syndrome.
• Heart Block: A conduction block can occur due to any obstruction in the normal pathway of the electrical conduction. Their anatomical location can be categorized as sinus node, atrioventricular node, or bundle branch blocks.
• Sinus node or sinoatrial exit block – occurs due to failed propagation of the impulses beyond SA node resulting in dropped P waves on the ECG. Common causes include sick sinus syndrome, increased vagal tone, inferior wall MI, vagal stimulation, myocarditis, drugs including digoxin, beta-blockers, etc.
• Atrioventricular or AV block – is a conduction block that can occur anywhere between the SA node and Purkinje fibers. There are three variants of AV blocks: first-degree, second-degree, and third-degree. Clinically significant points in diagnosing the AV blocks include careful measurement of the PR interval and examination of the relationship of the P waves to QRS complexes.
• First-degree heart block – is defined as prolongation of the PR interval by more than 200 milliseconds only. A single P wave precedes every QRS complex. It may be a normal finding in some individuals, but it can be an early sign of degenerative disease of the conduction system or a transient manifestation of myocarditis or drug toxicity, hypokalemia, acute rheumatic fever, etc. It usually does not require any treatment.[rx]
• Second-degree heart block – is of two types, i.e., Mobitz type I (also known as Wenkebach block) and Mobitz type II. In type I, the block across the AV node or bundle of His is variable and increases with each ensuing impulse, ultimately resulting in a drop of the impulse (usually every third or fourth impulse). On ECG, it shows as a progressive prolongation of the PR interval, and then suddenly, a P wave is not followed by the QRS complex. This sequence repeats itself in a regular manner. Most patients with Mobitz type I second-degree AV block are asymptomatic. Mobitz type I AV block may occur in the setting of acute myocardial ischemia or myocarditis and may also result in clinical deterioration if the resulting ventricular rate is inadequate to maintain cardiac output. Most patients with Mobitz type I second-degree AV block are asymptomatic and do not require any specific intervention. Rarely, patients with Mobitz type I block are symptomatic and demonstrate hemodynamic instability and may require treatment with either atropine (emergently) and eventually cardiac pacing. In type II  AV block, there is a dropped beat without the progressive lengthening of the PR interval. It follows the all-or-nothing phenomenon. It usually occurs below the AV node at the level of the bundle of His. It clinically signifies a severe underlying heart disease that can progress to third-degree heart block. When diagnosed, it usually requires prompt treatment with a permanent pacemaker.
• Third-degree heart block – is characterized by a complete electrical dissociation between the atria and ventricles, resulting in atria and the ventricles beat at their intrinsic rates. Degenerative disease of the conduction system is the leading cause of third-degree heart block. A complete heart block may present in acute myocardial infarction. Complete heart block may be reversible with prompt revascularization, especially in inferior MI. Lyme disease may be associated with a complete heart block and is potentially reversible with antibiotic therapy. In the case of irreversible or permanent complete heart block, a permanent pacemaker remains the mainstay of the treatment.
• Bundle branch block – results from the conduction block of either left or right bundle branches. It gets diagnosed by examining the width and configuration of the QRS complexes. The right bundle branch block is represented on the ECG by the presence of a widened QRS complex greater than 0.12 seconds along with an RSR pattern in V1 and V2. Also, there may be ST-segment depression and T wave inversions, and reciprocal changes in leads V5, V6, I, and aVL. Conduction system disorders can cause the right bundle branch block, but it may be present as a standard variant in specific individuals. The left bundle branch block is represented on the ECG by a widened QRS complex greater than 0.12 seconds, broad or notched R wave with prolonged upstroke in the leads V5, V6, I, and aVL, along with ST-segment depression and T wave inversion, and reciprocal changes in leads V1 and V2. Usually, a left axis deviation is also present. The left bundle branch usually signifies an underlying pathology, such as degenerative disease of the conduction system or ischemic heart disease.
• QRS COMPLEX: It represents ventricular depolarization as current passes down the AV node. A standard QRS complex has a duration of less than three small squares (under 120 ms, usually 60 to 100 ms). A prolonged QRS may indicate hyperkalemia or bundle branch block. A premature ventricular contraction or a ventricular rhythm can be associated with a wide QRS.
• SEPTAL Q-WAVE: Q-wave often appears as a tiny negative deflection in leads I, aVL, V5, and V6. It represents the depolarization of the interventricular septum. Its amplitude is not bigger than 0.1mV; that is why septal depolarization is not always visible on the EKG. Pathological Q-waves on EKG can signify an old infarct. A Q-wave duration of greater than 40 milliseconds (one small box), depth greater than 1 mm, or a size greater than 25% of the QRS complex amplitude is considered to be pathologic.[rx]
• R-WAVE: It is the tallest wave of the QRS complex, and it represents the electrical stimulus as it passes down the ventricles during depolarization. The R-wave progressively increases in amplitude moving right to the left in the precordial leads and is called R-wave progression. Lead V1 has the smallest R-wave, and lead V5 has the largest. A reduced R-wave progression has several causes, including prior anteroseptal MI, left ventricular hypertrophy or inaccurate lead placement, etc.[rx]
• S-WAVE: It represents the final depolarization of the Purkinje fibers. It is any downward deflection after R-wave. It may not be present in all ECG leads. S-wave is most significant in V1 and progressively becomes smaller to no S-wave in the lead V6.
• T-WAVE: It represents ventricular repolarization. Its morphology is highly susceptible to cardiac and noncardiac influences like ( hormonal, neurological). In leads with tall R-waves, it is usually positive (upward deflection). The suggested criteria for the typical T wave include the size of one-eighth or less than two-thirds of the size of the R wave and a height less than 10 mm. Abnormalities in the T-wave morphology can include inverted, flat, biphasic, or tall tented T-waves. T waves can be helpful in a variety of pathologies, tall T waves in anterior chest lead III, aVR, and V1 with a negative QRS complex may suggest acute myocardial ischemia.[rx] Other causes of T wave abnormalities are caused by physiological factors (e.g. postprandial state), endocrine or electrolyte imbalance, myocarditis, pericarditis, cardiomyopathy, postcardiac surgery state, pulmonary embolism, fever, infection, anemia, acid-base disorders, drugs, endogenous catecholamines, metabolic changes, acute abdominal process, intracranial pathology, etc.[rx]
• ST SEGMENT: It depicts the end of ventricular depolarization and the beginning of ventricular repolarization. The average duration of ST segment is less than 2 to 3 small squares (80-120ms). ST-segment is an isoelectric line and lies at the same level as PR-interval. Elevation or depression of the ST segment by 1mm or more, measured at J point, is considered abnormal. A J point is a region between the QRS complex and the ST segment. ST-elevation is highly specific if present in two or more contiguous leads in the setting of acute myocardial infarction. If the vertical distance on the ECG trace and the baseline at a point 0.04 seconds after the J-point is at least 1 mm in a limb lead or 2 mm in a precordial lead is clinically significant for the diagnosis of acute myocardial infarction. Correct ST segment interpretation is crucial as there is a type of ST-segment elevation present in healthy individuals that occurs due to early repolarization and is termed as J-point elevation. It is distinguished by the fact that the T wave does not merge with the ST segment and remains an independent wave. Several other disorders are also associated with ST-elevation, i.e., Prinzmetal angina, acute pericarditis, acute myocarditis, hyperkalemia, blunt trauma, pulmonary embolism, subarachnoid hemorrhage, Brugada syndrome, ventricular aneurysm, and left bundle branch block.[rx][rx][rx] ST-elevations are diffuse in acute pericarditis and associated with PR-depression in reference to TP-segments (except for leads V1 and aVR).[rx][rx][rx][rx]. In myocardial infarction, the ST elevation tends to be localized (inferior, anterior, posterior, lateral), often, but not always with reciprocal ST depression.[rx] Second, the PR segment displacement, which is attributable to the subepicardial atrial injury. PR elevation can present in aVR, and PR depression is best seen in II, aVF, V4-V6. PR-depression and slight downsloping appearance of TP segments are often known as Spodick’s sign of pericarditis and help distinguish acute pericarditis from acute MI.[rx] ST depression greater than 1 mm is often a sign of myocardial ischemia or angina. It can appear as a downsloping, upsloping, or horizontal segment on the ECG. A horizontal or downsloping ST depression greater than 0.5 mm at the J-point in two or more contiguous leads indicates myocardial ischemia. An upsloping ST depression in the precordial leads with prominent De Winter T waves is highly indicative of MI caused by occlusion of the left anterior descending artery.[rx] ST depression can represent a reciprocal change with a morphology that resembles “upside-down” ST elevation and typically seen in leads electrically opposite to the site of infarction. For example, posterior wall MI manifests as horizontal ST depression in leads V1-3 and is associated with tall R waves and upright T waves. Likewise, inferior wall STEMI produces reciprocal ST depression in leads I and aVL, and there is often a reciprocal ST-depression in leads III and aVF in lateral wall MI.[rx] ST depressions are also associated with several non-ischemic causes, including digoxin toxicity, hypokalemia, hypothermia, and tachycardia.[rx]
• QT INTERVAL: It represents all start of depolarization to the end of repolarization of ventricles. The normal QT interval duration is somewhat controversial, and various normal durations have been previously suggested. In general, the normal QT interval is less than 400 to 440 milliseconds (ms), or 0.4 to 0.44 seconds. Women usually have a slightly longer QT interval than men. A QT interval has an inverse relation to the heart rate. A prolonged QT interval presents an imminent risk for serious ventricular arrhythmias, including Torsades de Pointes, ventricular tachycardia, and ventricular fibrillation. A common cause of QT prolongation includes medications, electrolyte abnormalities such as hypocalcemia and hypomagnesemia and congenital long QT syndrome.[rx]A short QT interval ( less than 360 milliseconds) may be present associated with hypercalcemia, acidosis, hyperkalemia, hyperthermia, or short QT syndrome.[rx]
• U WAVE:  It is a small wave that follows the T wave. It represents the delayed repolarization of the papillary muscles or Purkinje fibers. It is commonly associated with hypokalemia.
• J WAVE: also known as Osborn wave, is an abnormal EKG finding in hypothermia. It appears as an extra deflection on ECG at the junction of the QRS complex and ST-segment.[rx]
• EPSILON WAVE: It is a small positive deflection usually found buried at the end of the QRS complex as a characteristic finding in arrhythmogenic right ventricular dysplasia.[rx]

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• https://en.wikipedia.org/wiki/Concrete_slump_test
• https://www.sciencedirect.com/science/article/abs/pii/S0263931918300693
• https://en.wikipedia.org/wiki/Neurological_examination
• https://en.wikipedia.org/wiki/Back_examination
• https://www.spineuniverse.com/exams-tests/diagnosing-back-or-neck-pain-physical-examination

• https://www.ncbi.nlm.nih.gov/books/NBK431071/
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• https://www.ncbi.nlm.nih.gov/books/NBK545299/
• https://www.ncbi.nlm.nih.gov/books/NBK525969/
• https://www.ncbi.nlm.nih.gov/books/NBK525969/
• https://www.ncbi.nlm.nih.gov/books/NBK493152/
• https://www.ncbi.nlm.nih.gov/books/NBK519492/
• https://www.ncbi.nlm.nih.gov/books/NBK560721/
• https://www.ncbi.nlm.nih.gov/books/NBK557604/
• https://www.ncbi.nlm.nih.gov/books/NBK562179/
• https://www.ncbi.nlm.nih.gov/books/NBK544267/
• https://www.ncbi.nlm.nih.gov/books/NBK519066/
• https://www.physio-pedia.com/Slump_Test
• https://en.wikipedia.org/wiki/Yeoman’s_test
• https://en.wikipedia.org/wiki/Slump_test
• https://en.wikipedia.org/wiki/Concrete_slump_test
• https://www.sciencedirect.com/science/article/abs/pii/S0263931918300693
• https://en.wikipedia.org/wiki/Neurological_examination
• https://en.wikipedia.org/wiki/Back_examination
• https://www.spineuniverse.com/exams-tests/diagnosing-back-or-neck-pain-physical-examination

Plasmapheresis is a therapeutic intervention that involves extracorporeal removal, return, or exchange of blood plasma or components. The underlying mechanism of this procedure is accomplished by either centrifugation or filtration using semipermeable membranes. This activity reviews plasmapheresis as a therapeutic intervention that involves extracorporeal removal, return, or exchange of blood plasma or components. This intervention results in a filtered plasma product that can be used for the treatment of numerous diseases. It also highlights the interprofessional team strategies for improving care coordination and communication to advance plasmapheresis and improve outcomes.

Plasmapheresis is a therapeutic intervention that involves extracorporeal removal, return, or exchange of blood plasma or components.[rx][rx] The underlying mechanism of this procedure is accomplished by either centrifugation or filtration using semipermeable membranes. While centrifugation is based on the principle of separation using different specific gravities of various blood components, membrane plasma separation filters blood components based on their particle size.[rx][rx]

The preferred method of plasmapheresis in most centers worldwide is by automated centrifuge-based technology.[rx] However, in certain hospitals and patients on hemodialysis, plasmapheresis is done using membrane plasma separation.[rx] In plasmapheresis using centrifugation, filtered plasma is discarded, and RBCs and replacement fluid (donor plasma or colloids) are returned. Membrane plasma separation allows selective removal of undesired macromolecules; hence, filtered, processed plasma is returned to the patient, eliminating the need for replacement fluids.

Indications 0f Plasmapheresis

Therapeutic plasmapheresis is used for numerous diseases. The conditions involve the presence of a toxic substance in plasma (e.g., immunoglobulin), which can be filtered. The disorders where therapeutic plasmapheresis can be done are grouped into four categories by the Apheresis Applications Committee of the American Society for Apheresis (ASFA). Category 1 includes disorders where plasmapheresis can be done as a first-line treatment, category 2 includes disorders where plasmapheresis can be done as a second-line treatment in addition to the existing standard of care, category 3 includes disorders in which the evidence of the benefit of plasmapheresis is minimal, and therapy must be individualized, and category 4 includes disorders in which the evidence suggests that plasmapheresis is either ineffective or harmful, however, may be considered after approval from the institute ethics committee.[rx]

The alphabetical list of various indications for plasmapheresis, along with their ASFA category, is as follows.

Category 1

• Acute inflammatory demyelinating polyradiculoneuropathy/Guillain-Barre syndrome
• ANCA-associated rapidly progressive glomerulonephritis (dialysis-dependent or associated with diffuse alveolar hemorrhage)
• Anti-glomerular basement membrane disease-Goodpasture syndrome (dialysis independent or associated with diffuse alveolar hemorrhage)
• Chronic inflammatory demyelinating polyradiculoneuropathy
• Focal segmental glomerulosclerosis (recurrent in the transplanted kidney)
• Hyperviscosity in monoclonal gammopathies
• Liver transplantation: Desensitization
• Myasthenia gravis
• N-methyl D-aspartate receptor antibody encephalitis
• Paraproteinemic demyelinating neuropathies/chronic acquired demyelinating polyneuropathies (IgA/IgG/IgM mediated)
• Progressive multifocal leukoencephalopathy associated with natalizumab
• Renal transplantation: Desensitization and antibody-mediated rejection
• Thrombotic microangiopathy (Factor H autoantibodies and ticlopidine)
• Thrombotic thrombocytopenic purpura
• Wilson disease (fulminant)

Category 2

• Acute disseminated encephalomyelitis
• Cardiac transplantation: Desensitization
• Catastrophic antiphospholipid syndrome
• Cryoglobulinemia; symptomatic/severe
• Dilated cardiomyopathy, idiopathic (NYHA 2-4)
• Hashimoto encephalopathy: Corticosteroid responsive encephalopathy associated with autoimmune thyroiditis
• Hematopoietic stem cell transplantation, ABO-incompatible
• Lambert-Eaton myasthenic syndrome
• Multiple sclerosis
• Myeloma cast nephropathy
• Neuromyelitis Optica spectrum disorders
• Overdose, envenomation, and poisoning, such as mushroom
• Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)
• Phytanic acid storage disease (Refsum disease)
• Systemic lupus erythematosus (severe)

Category 3

• Acute liver failure
• ANCA-associated rapidly progressive glomerulonephritis (dialysis independent)
• Anti-glomerular basement membrane disease, Goodpasture syndrome (dialysis-dependent, no DAH)
• Aplastic anemia, pure red cell aplasia
• Autoimmune hemolytic anemia
• Burn shock resuscitation
• Cardiac neonatal lupus
• Cardiac transplantation: Antibody-mediated rejection
• Chronic focal encephalitis (Rasmussen encephalitis)
• Complex regional pain syndrome; chronic
• Erythropoietic porphyria, liver disease
• Hemolysis liver enzymes low platelet (HELLP) syndrome (postpartum)
• Hematopoietic stem cell transplantation, HLA desensitization
• Hemophagocytic lymphohistiocytosis; hemophagocytic syndrome; macrophage activating syndrome
• Henoch-Schonlein purpura
• Heparin-induced thrombocytopenia and thrombosis
• Hypertriglyceridemic pancreatitis
• Immune thrombocytopenia; refractory
• IgA nephropathy; crescentic
• Lung transplantation: Desensitization and antibody-mediated rejection
• Paraneoplastic neurological syndromes
• Pemphigus Vulgaris; severe
• Pruritus due to hepatobiliary diseases
• Scleroderma (systemic sclerosis)
• Sepsis with multiorgan failure
• Stiff-person syndrome
• Thrombotic microangiopathy (complement factor gene mutations, MCP mutations, clopidogrel, and calcineurin inhibitors)
• Thyroid storm
• Toxic epidermal necrolysis (refractory)
• Vasculitis
• Voltage-gated potassium channel antibodies

Category 4

• Amyloidosis, systemic
• Dermatomyositis/polymyositis
• HELLP syndrome (antepartum)
• Lupus nephritis
• Thrombotic microangiopathy (gemcitabine and quinine)

Contraindications of Plasmapheresis

The contraindications for therapeutic plasmapheresis are as follows:[rx]

• Non-availability of central line access or large bore peripheral lines
• Hemodynamic instability or septicemia
• Known allergy to fresh frozen plasma or replacement colloid/albumin
• Known allergy to heparin
• Hypocalcemia (restricts the use of citrate as an anticoagulant during the procedure); relative contraindication
• Angiotensin-converting enzyme (ACE) inhibitor used in last 24 hours; relative contraindication

Equipment

Venous access for this procedure is either by a central venous catheter or large bore peripheral lines. There are multiple manufacturers of centrifuge-based plasmapheresis machines.

Another technique of performing plasmapheresis is by using semipermeable membrane filters with a standard hemodialysis machine. However, for this technique, central venous access is mandatory due to the need for higher blood flow rates of 100 mL/min to 150 mL/min. There are two membrane-based technologies that are currently available; hollow fiber and parallel plate. Hollow fiber dialyzers are cylindrical shell-like structures, consisting of multiple polysulfone capillary fibers.

Parallel plate dialyzers consist of layered membranes, with ridges and grooves which facilitate filtration. Both these dialyzers allow plasma filtration based on particle size and pressure gradients. Hollow fiber dialyzers are more gentle as opposed to parallel plate dialyzers and are preferred for pediatric patients, whereas hollow fiber dialyzers use less blood volume, and hence require a reduced dose of citrate or heparin for anticoagulation.

The major advantage of membrane-based plasmapheresis over centrifuge-based technology is that the removed processed plasma by ultrafiltration can be returned to the patient eliminating the need for replacement fluids or colloids.[rx]

Personnel

Plasmapheresis was traditionally performed in blood banks by centrifuge-based techniques. However, therapeutic plasmapheresis procedures are routinely performed by critical care specialists in the intensive care unit, nephrologists, and dialysis-technicians after specialized skill-based training.

Preparation

No specific patient preparation is needed for this procedure. However, while inserting a central line, a local anesthetic may be needed. For this purpose, 2% lidocaine injection is used routinely. In pediatric patients, sedation with opioids and benzodiazepines may be considered for pain and anxiety control.

The patient is positioned supine for plasmapheresis; however, the position, especially of the neck, maybe altered according to the location of central venous access to maintain adequate blood flow throughout the procedure.

A close watch on patient vitals is recommended throughout the procedure to assess for volume depletion, hypocalcemia, and complications of fresh frozen plasma transfusion.

Technique

The steps for performing plasmapheresis using centrifuge-based equipment are as follows:[rx]

• Initially, a waste of around 3-5 mL of blood from the central venous catheter is discarded.
• After drawing baseline samples for complete hemogram, calcium, and fibrinogen, it is flushed with 5-10 mL of heparinized saline.
• The double lumen catheter is now connected to the machine tubing to start the priming procedure.
• The machine calculates the total body volume (TVB), and the effective plasma volume (which equals TVB × (1 – hematocrit)) of the patient based on the operator’s entered height and weight.
• The replacement product to be used and its desired volume (40 – 60 mL/kg) is decided by the clinician, and entered into the machine, based on which it calculates the centrifuge speed.
• The separated plasma is discarded by the machine, and the RBCs are returned back to the patient along with the replacement fluid.
• Finally, post-procedure, tubings are connected to heparinized saline, and reinfusion is initiated.
• Post-plasmapheresis blood for fibrinogen and calcium is sent again, and lumens of central venous catheters are flushed.

• https://www.ncbi.nlm.nih.gov/books/NBK499824/
• https://www.ncbi.nlm.nih.gov/books/NBK269390/
• https://www.ncbi.nlm.nih.gov/books/NBK499929/
• https://www.ncbi.nlm.nih.gov/books/NBK482202/
• https://www.ncbi.nlm.nih.gov/books/NBK327570/
• https://www.ncbi.nlm.nih.gov/books/NBK564300/
• https://www.ncbi.nlm.nih.gov/books/NBK539826/
• https://www.ncbi.nlm.nih.gov/books/NBK2265/
• https://www.ncbi.nlm.nih.gov/books/NBK563179/
• https://www.ncbi.nlm.nih.gov/books/NBK448158/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5620780/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4296418/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7648522/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4724982/
• https://www.ncbi.nlm.nih.gov/books/NBK560566/
• https://www.nhs.uk/conditions/blood-transfusion/
• https://www.nhlbi.nih.gov/health-topics/blood-transfusion
• https://en.wikipedia.org/wiki/Blood_transfusion

Contraindications of Blood Transfusions

Articles on Patient Blood Management outline the decision-making process required before transfusing a patient.  Significant contraindications that merit consideration include the risk of transfusion in a patient who is volume overloaded or who has previously had a reaction to blood.[rx]   Another important consideration is to avoid transfusion of blood without prior compatibility testing and antibody screening unless it is an emergency.

Equipment

Per the American Association of Blood Banks, all blood bags and needles are sterile, used only once, and then discarded to avoid contamination from donor to donor that could later affect multiple recipients of transfusion. The equipment used for blood donation collection such as blood pressure monitors, scales, blood collection monitors/mixers, blood bag tube sealers, transportation boxes, and refrigerators are calibrated, cleaned, and serviced routinely. The chairs and couches used in the area of blood donation are to be of cleanable surfaces such as vinyl. Transport supplies and containers are also cleanable according to the World Health Organization guidelines. All blood bags should undergo routine inspection for sterility, expiration date, appearance, and any evidence of leakage or defects at the time of donation collection.

Personnel

Phlebotomy and collection should be via qualified personnel trained in blood donation. Donation monitoring is under the overall responsibility of a medical practitioner or authorized personnel who can manage blood donor adverse reactions.  Blood transfusion into patients is also performed with adequate oversight and under the purview of a medical practitioner or other qualified health care professional.  Real-time monitoring of patients during transfusion ensures that accurate information is available for the detection and work-up of suspected transfusion reactions. Laboratory technologists are trained and educated on the importance of appropriate testing for possible infectious agents before transfusion, blood group and compatibility, potential antibodies, and post-transfusion evaluations for hemolysis. Transfusion service personnel who are committed to following accepted guidelines and to determining and auditing thresholds for transfusion have significantly influenced blood product safety.

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.[rx] 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.[rx][rx] 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.[12] 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.[rx] 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.[rx]

Technique

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.[rx][rx]   “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.[rx][rx] 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.[rx]  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).[rx][rx]  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.[rx]  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.[rx]   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.

• https://www.ncbi.nlm.nih.gov/books/NBK499824/
• https://www.ncbi.nlm.nih.gov/books/NBK269390/
• https://www.ncbi.nlm.nih.gov/books/NBK499929/
• https://www.ncbi.nlm.nih.gov/books/NBK482202/
• https://www.ncbi.nlm.nih.gov/books/NBK327570/
• https://www.ncbi.nlm.nih.gov/books/NBK564300/
• https://www.ncbi.nlm.nih.gov/books/NBK539826/
• https://www.ncbi.nlm.nih.gov/books/NBK2265/
• https://www.ncbi.nlm.nih.gov/books/NBK563179/
• https://www.ncbi.nlm.nih.gov/books/NBK448158/
• https://www.nhs.uk/conditions/blood-transfusion/
• https://www.nhlbi.nih.gov/health-topics/blood-transfusion
• https://en.wikipedia.org/wiki/Blood_transfusion

Many hospitals and health systems have removed the test without any demonstrated harm. In most cases, a thorough history and physical is the only workup needed for the pre-operative assessment of bleeding risk. When the clinical effectiveness of platelet aggregation is desired, a modern platelet function assay can provide the necessary information. This is being increasingly utilized in intracranial hemorrhage on various antiplatelet agents prior to pooled platelet transfusion.

Specimen Collection

While measuring the bleeding time requires trained personnel, no gross specimen collection is necessary. Modern alternative platelet function analyzers require a small aliquot of peripheral blood. Technicians utilize standardized instruments to perform and interpret the test.

Procedures

This test is performed via two primary methods based on the length and location of the incision.

The IVY method is the most common. The patient’s arm is positioned at the level of the heart, and a blood pressure cuff inflated to 40 mmHg. After cleansing with alcohol, a standardized device is utilized to make a 10mm long and 1mm deep incision on the volar forearm. Using a timer the blood is blotted twice a minute. The time stops when there is no further bleeding after blotting.

The Duke method involves a stab incision in the patient’s cleaned finger or earlobe with a lancet. Otherwise, the methodology is the same.

The IVY method is more accurate but has an increased scarring risk. The Duke method is less accurate and carries a higher hematoma rate.

Either method carries the risks of infection and bleeding. In addition, the discomfort is not insignificant. Different normal ranges exist for each method further confounding the interpretation of results by lay clinicians.

Indications

The measurement of bleeding time is mostly of historical value in the screening of qualitative platelet abnormalities. It was used to screen for bleeding disorders and quantify platelet function in patients taking aspirin or non-steroidal anti-inflammatory medications. The American College of Clinical Pathologists position statement identifies a carefully conducted clinical history that includes family and previous dental, obstetric, surgical, traumatic injury, transfusion, and drug histories as the best predictor of bleeding risk.[rx] As most hospitals and laboratories have removed this exam from their offerings, it has fallen out of regular use. Most current uses are likely grounded in physician preference rather than clinical research.

Potential Diagnosis

• Thrombocytopenia

  • Decreased platelet count impairs primary hemostasis. Sepsis, drug reactions, hematologic malignancies, autoimmune conditions, and vitamin deficiencies are among the non-inherited causes. Spontaneous bleeding is not generally a problem seen until counts fall beneath 30,000.
• Von Willebrand Disease (vWD)

  • Von Willebrand disease is an inherited deficiency in the quantity or function of the platelet aggregation protein Von Willebrand factor. Rather than bleeding time,  modern workup includes complete blood count, factor VIII levels, ristocetin cofactor activity, and GP-Ib binding assay.
• Disseminated Intravascular Coagulation (DIC)

  • DIC is a symptom of other severe disease processes like sepsis, burns, trauma, pregnancy, and malignancy. The coagulopathy is consumptive from the formation of blood clots throughout the peripheral vasculature. Thrombocytopenia with low fibrinogen and a high INR are the classic laboratory abnormalities.
• Glanzmann’s

  • Glanzmann’s thrombasthenia is an autosomal recessive inherited defect in the fibrinogen binding receptor glycoprotein IIb/IIIa.
• Bernard-Soulier Disease

  • Bernard-Soulier Syndrome is a rare autosomal recessive genetic defect in glycoprotein Ib causing giant platelets with perceived thrombocytopenia. Platelet transfusion is the treatment of choice.
• Platelet Function Inhibiting Medications (aspirin, clopidogrel, ticagrelor, etc.)

  • Aspirin and other novel antiplatelet agents inhibit platelet aggregation and secretion overall inhibiting their function.

Normal and Critical Findings

Normal bleeding time:

• Duke – Less than 3 minutes
• IVY – Less than 8 minutes

Times greater than 5 minutes in the Duke method and 10 minutes in the IVY method are concerning for coagulopathy. Abnormalities would require further evaluation with a focus on the coagulation pathway of interest.

• https://www.ncbi.nlm.nih.gov/books/NBK470328/
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• https://www.ncbi.nlm.nih.gov/books/NBK547705/
• https://en.wikipedia.org/wiki/Platelet
• https://www.redcrossblood.org/donate-blood/dlp/platelet-information.html
• https://www.sciencedirect.com/topics/medicine-and-dentistry/platelet
• https://en.wikipedia.org/wiki/Thrombocytopenia

An ileostomy is a surgery that makes a temporary or permanent opening called a stoma. A stoma is a pathway from the lowest part of the small intestine, called the ileum, to the outside of your abdomen. This helps solid waste and gas exit the body without passing through the colon or the rectum.

An ileostomy is a procedure in which the lumen of the ileum, part of the small bowel, is brought through the abdominal wall via a surgically-created opening called a stoma. The purpose of an ileostomy is to evacuate stool from the body via the ileum instead of the usual route via the anus. This activity reviews the indications, contraindications, and potential benefits of the ileostomy and highlights the role of the interprofessional team in the management of patients with a stoma.

An ileostomy is when the lumen of the ileum (small bowel) is brought through the abdominal wall via a surgical opening (created by an operation). This can either be temporary or permanent, an end or a loop. The purpose of an ileostomy is to evacuate stool from the body via the ileum rather than the usual route of the anus. The output from an ileostomy consists of loose or porridge-like stool consistent with that expected to pass through the small bowel (as it is the large bowel that is responsible for making the stool more solid dependent upon water absorption). The output from an ileostomy can vary but typically ranges from 200 to 700 ml per day, and an Ileostomy is typically formed on the right side of the abdomen.

Anatomy and Physiology

An ileostomy is formed from a section of the ileum which is part of the small intestine. The small intestine begins at the pylorus of the stomach and is composed of three adjoining sections: the duodenum proximally, jejunum, and the ileum distally. The jejunum and ileum are intraperitoneal structures whereas the duodenum has a retroperitoneal component to it. The jejunum and duodenum are attached to the small bowel mesentery which are peritoneal folds containing blood vessels, lymphatics, and nerves. The small intestine is approximately 6 to 7 meters in length with a varying luminal diameter between 3 and 5 cm. It has multiple functions including food digestion, secretion of enzymes and proteins, and nutrient absorption [rx]. The wall of the intestine consists of the mucosa, the submucosa, muscularis propria (the muscular layer), the subserosa, and finally the serosa [rx]. The ileum terminates at the ileocaecal junction in a valve at the superior aspect of the caecum before it goes on to form the ascending colon. The caecum can be identified at this point of the bowel where the tinea converge.

The anatomy of the anterior abdominal wall is important to be aware of when forming the trephine incision for the ileostomy. The layers encountered are the skin, subcutaneous fat, Scarpa’s and Camper’s fascia, anterior rectus sheath, muscle, posterior rectus sheath (if above the arcuate line), and the peritoneum. The muscles include the external and internal obliques, the transverse abdominis, and the rectus abdominis. The obliques and transverse abdominis attach at varying levels to the lower ribs and the iliac crests, whereas the rectus abdominis arises from the costal margin and xiphoid process before extending down to the symphysis pubis. The abdominal muscles are wrapped in fascia but also have dense tendons called aponeuroses that converge at the midline to form the linea alba.

An ileostomy should be brought through the rectus muscle and sheath to reduce the risk of laterparastomal hernia formation, which occurs when the abdominal content pushes through the weakness created by the incision.

Indications

There are different indications for forming an ileostomy but essentially arrive at the same result of diverting stool out of the body without it ever entering the colon.

A loop ileostomy is when a distal loop of the ileum is brought out to the skin with 2 lumens draining into the stoma bag and is commonly used as a temporary diversion of stool usually to protect a distal anastomosis such as a colonic anastomosis in segmental colonic resections. The reason to protect such distal anastomoses is to reduce the risk of an anastomotic leak from when stool passes through the joint of the two ends of the bowel [rx]. Once the distal anastomosis has healed, both limbs of the loop ileostomy can be joined back together thereby restoring continuity to the gastrointestinal tract, which allows stool to pass through into the colon. With loop ileostomies, the proximal limb is the one that passes out the stool, and the distal limb usually acts as a mucous fistula, draining out the secretions produced within the mucosal lining from the lumen to the caecum. However, the distal limb does not drain out colonic secretions if the ileocaecal valve is competent, and therefore, does not decompress the colon. This is important to note if there is a colonic obstruction as then the patient would be at risk of perforation from a large bowel obstruction. This is because the colon is unable to decompress either proximally or distally to the obstructing source, causing secretions and flatus to build up under tension in an essentially closed loop of the bowel. At a later date, usually between three and six months, this temporary ileostomy can be “reversed” or re-joined back together to re-establish continuity of the bowel.

An end ileostomy is when there is nothing distal to the proximal emptying limb, in other words, there is no bowel to be re-attached to this “end” at a later stage. The formation of an end ileostomy is usually considered following permanent removal of the entire colon, and therefore the patient manages their stoma for the rest of their life.

In brief, the indications for forming an ileostomy include:

• To defunction the rest of the bowel in order to protect a distal anastomosis
• To evacuate stool from the body if the entire colon has been removed such as in colorectal cancer, Crohn’s disease, ulcerative colitis, and familial adenomatous polyposis
• Relieve bowel obstruction

Contraindications

There are no absolute contraindications to ileostomy formation, but the relative ones include:

• Short mesentery disables the ileum from being exteriorized through the abdominal wall to the skin without tension. This, unfortunately, is more common in obese patients.
• Carcinomatosis that prevents full mobilization of the ileum

The ileostomy should be formed as distal as possible to allow enough bowel length for absorption of nutrients.

A high output ileostomy can lead to electrolyte disturbances (particularly important to monitor for and treat in patients with renal impairment), as well as malabsorption leading to malnutrition.

During ileostomy formation, it is important to spout the stump to get the effluent away from contact with the skin.

An ileostomy should be sited away from scars, skin creases, and bony prominences to allow placement of the stoma appliance and avoid leakage.

Equipment

The equipment required can be split into the operative stage and the maintenance stage. In the operative stage, the formation of the trephine ileostomy involves the utilization of many instruments that are discussed below in the technique section. The maintenance stage is based on stoma education and how the patient manages their ileostomy. This includes the use of stoma bags, perhaps extra adhesive fixings such as spray, powder, paste, and rings, as well as belts, adhesive removal spray, wet wipes, and waste disposal bags.

Preparation

This includes both physical and psychological elements of preparation; the stoma nurses are again invaluable here to help support the patient through this process. Physical preparation varies somewhat on the nature of the operation involved and whether it is an emergency procedure or a planned elective operation.

Points to consider include

• Shaving of hair on the abdominal wall
• Body mass index (BMI) of patients having a planned ileostomy in an elective setting: They may be asked to lose weight prior to the operation to not only improve their anesthetic suitability but also reduce the distance the small bowel mesentery has to traverse to be bought to the skin without being under tension.
• Previous operative scars/deformities of the abdominal wall. A previous operation increases the extent of adhesions
• The presence of herniae
• Also in a planned setting, one would consider the effect of smoking and diabetic control on wound healing
• Most importantly would be the positioning of the stoma site, which is usually on the right side of the abdomen at the lateral edge of the rectus muscle, at a level where the patient can see it, access it easily, and not have it interfering with belts or skin folds. It should also ideally avoid the coastal margin and umbilicus.
• A nasogastric tube in cases of obstruction/perforation or if anticipating a postoperative ileus
• Adequate fluid and electrolyte resuscitation.

Technique

Ideally, the site would be marked pre-operatively with indelible ink or an “X” scored into the skin. This is so that the site can still be seen at the end of a long operation when the antiseptic prep or blood may have distorted the skin. If a laparotomy has been formed then the linea alba, which is the cut edge of the abdominal wall, is grasped with Kocher clamps or Littlewood clamps and retracted toward the midline to approximate the two wound edges together. As this will be the anatomically correct position of closure of the abdominal wall, it will also help identify where the ileostomy will be sited once the wound is closed. If a loop ileostomy is being made laparoscopically, then under vision the ileum can be grasped with a pair of Johan atraumatic graspers and bought towards the anterior abdominal wall to sit in a position where it is not under tension.

A 2.5 to 3 cm circle or ellipse of skin is excised using monopolar diathermy (it may be helpful to lift the skin upward using an Alice clamp or Littlewood clamp). The tissue is then dissected down through the subcutaneous fat to the anterior fascial sheath of the rectus muscle, which is then opened through a cruciate incision. The rectus muscle is spread or retracted medially; however, caution must be taken to avoid injuring the epigastric vessels that run deeply in the center of this muscle. Once the muscle is retracted, the posterior sheath is seen underlying this which is usually closed attached to the peritoneum on its under-surface. Another cruciate incision is made to the posterior sheath, and then two Kelly clips are used to grasp the peritoneum and lift it up. Using dissection scissors, a cut is made in the peritoneum between the two clips which will gain access into the peritoneal cavity. The surgical defect is stretched to allow two fingers to traverse through it thus ensuring enough room for the small bowel to be bought up to form the ileostomy. The next step is to gently pass the selected segment of terminal ileum (which has been checked to have enough length, mobilization, and is tension-free) through the trephine that you just formed. If a loop ileostomy is being formed, it is the loop of ileum that is bought up through the abdominal wall defect to the skin. If an end ileostomy is being formed, then it is simply the stapled off the end of ileum that is bought up. The ileum should be positioned such that the proximal limb is cephalad and is at 12 o’clock. It should also protrude approximately 5 cm above the skin before a seromuscular absorbable stay suture (e.g., 3.0 monocryl or vicryl rapide) is placed on the skin to prevent the ileum from slipping back inside. This then allows you to perform your final checks (checking orientation, controlling hemostasis, washout, rectus sheath catheters, drains) prior to closing up the abdomen and protecting the wounds with dressings before focussing on the ileostomy formation. It is considered common practice to close any abdominal wounds prior to the formation of the ileostomy so as to prevent fecal contamination of the wound with stool from the ileum.

Loop Ileostomy Formation

The distal limb is opened transversely for two-thirds of its diameter in a position about halfway up from the skin level. Submucosal bleeding can be controlled with bipolar cautery. Interrupted absorbable sutures are placed at the 3, 9, and 12 o’clock position taking seromuscular bites at the lumen of the proximal limb as well as approximately 4 cm down the loop before taking a subcuticular bite of the skin at the trephine skin edge. The positions here are away from the supplying mesentery. A Langenbeck retractor can then be used to help evert the lumen so that the limb is now spouting. The interrupted sutures are then tied in place using square knots. The distal limb is also everted similarly, however, will be less spouted as there is less protrusion of the distal limb above skin level. Interrupted absorbable sutures are applied circumferentially around both limbs, taking care not to compromise the vascular supply of the mesentery.

End Ileostomy

The formation of the trephine is the same here as mentioned above. Once you pull the stapled end of the ileum through the abdominal wall defect and apply the stay suture, you still proceed to carry out the usual checks and close the wounds as previously mentioned. Then taking the monopolar diathermy, you excise the staple line from the ileal end and discard it. Some surgeons may choose to cut the staple line off using dissecting scissors. However, this increases the risk of bleeding from the cut edges of the bowel which can be troublesome at times to control. Once the staple line has been excised, open up the lumen and then apply the 3 interrupted absorbable sutures at the 3, 9, and 12 o’clock position taking seromuscular bites. Again using a Langenbeck retractor, evert the mucosa of the lumen so that the limb is now spouting. The interrupted sutures are then tied in place using square knots.

What should I expect during surgery?

You will receive general anesthesia before the surgery. The procedure may be done with:

• A surgical incision, which is a large cut in the abdomen
• Laparoscopic surgery, which involves less invasive small incisions. This method reduces pain and recovery time.
• Bleeding inside the small intestine or from the stoma
• Damage to nearby organs
• Infection
• Not being able to absorb enough nutrients from food
• Intestinal blockage caused by scar tissue

How long will it take to recover from surgery?

Most patients stay in the hospital for up to 1 week after the procedure. Complete recovery from an ileostomy may take up to 2 months. During this time, you will have limits on what you can eat while the small intestine heals.

If the ileostomy is temporary, you may need a reversal, or closure, surgery after the small intestine has healed. This surgery usually takes place about 12 weeks later.

Ileostomy care

Emptying your ileostomy bag – Once you have recovered from surgery, you will need to empty the ileostomy bag several times per day. You will not be able to control when stool and gas move into the pouch. It is best to empty it when the bag is less than half full.

Ileostomy pouches come in many sizes and shapes, but there are 2 main types:

• One-piece pouches attach directly to the skin barrier.
• Two-piece pouches include a skin barrier and a pouch that can detach from the body.

Most pouches are drained through an opening in the bottom. Ask your health care team about which type of ileostomy pouch you will receive and instructions on how to empty it.

Draining waste with a catheter – If you have a continent ileostomy, the surgeon will leave a tube in the pouch so the waste can drain continuously, called an indwelling catheter. This will last for about 3 to 4 weeks. Once the indwelling catheter is removed, you will need to drain the pouch several times a day. This frequency will decrease over time.

Caring for your skin – The skin surrounding the stoma is called peristomal skin. It will always look red and may bleed occasionally, which is normal. However, bleeding should not continue for long.

It is important to make sure your pouch is correctly connected to your stoma. A pouch that fits poorly can irritate your skin. You should also keep this area clean and dry. If this skin appears wet, weepy, bumpy, itchy, or painful, it may be infected. Contact your healthcare team.

Ileostomy concerns

High stool output – During the first few days after surgery, you may have a larger than normal stool output. As your body gets used to the stoma and ileostomy, this amount will decrease. If it does not decrease after a few days, call your health care team. Passing large amounts of stool means you may be losing too many fluids. This could lead to an imbalance in your electrolyte levels. Electrolytes are minerals that help regulate the body.

Managing gas – Just like with stool, you will also need to release gas from your ileostomy pouch. The way you do this depends on the type of pouch. Some pouches have a filter that deodorizes and vents gas. This prevents the bag from becoming too stretched, coming off of the abdomen, or bursting.

Amounts of gas deposited into the pouch will vary based on the type of ileostomy and your diet. Foods and drinks such as beans, onions, milk, and alcohol can cause excess gas. Swallowing air can also increase the amount of gas in your small intestine. This happens when you chew gum or drink through a straw. You may have a lot of gas right after surgery. But this should decrease as your body heals. Your health care team can provide information on food and lifestyle choices to help reduce gas.

Whole pills or capsules in the stool – Coated pills and extended-release capsules may come out intact in your pouch. This can mean that the medication was not fully absorbed in your body. Tell your health care team if this happens. They may be able to prescribe liquid or gel medications for you to take instead.

Stoma obstruction – Sometimes your stoma may become blocked by a piece of undigested food and scar tissue. This means that stool and gas cannot pass through into the pouch. An obstruction may cause abdominal pain or swelling or nausea or vomiting.

You may be able to remove the blockage at home. This can be done by avoiding solid foods and drinking more fluids, including warm drinks like tea. You can also try massaging your abdomen around the stoma or drawing your knees to your chest and rocking side to side. If these tips do not work, call your health care team right away.

Complications

These can be classified as immediate, early, or late or as procedure-specific and general complications. It is important to note that complications following the creation of an intestinal stoma are experienced by 20% of the patients. General complications vary depending on the type of operation being undertaken for an ileostomy to be necessary. Procedure-specific complications include the following [rx]:

• Stenosis
• Ischemia/Necrosis
• Hemorrhage
• Infection/Abscess
• A parastomal hernia
• Retraction/Prolapse
• Electrolyte imbalance due to the high output of the effluent from the ileostomy
• Dehydration
• Renal impairment
• Hematoma/Seroma
• Obstruction
• Fistula formation
• Skin irritation

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