Category Archive Health

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• https://www.ncbi.nlm.nih.gov/books/NBK539717/
• 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

A lipoprotein is a biochemical assembly whose primary function is to transport hydrophobic lipid (also known as fat) molecules in water, as in blood plasma or other extracellular fluids. They consist of a Triglyceride and Cholesterol center, surrounded by a phospholipid outer shell, with the hydrophilic portions oriented outward toward the surrounding water and lipophilic portions oriented inward toward the lipid center. A special kind of protein, called apolipoprotein, is embedded in the outer shell, both stabilizing the complex and giving it a functional identity that determines its fate.

Lipoproteins are complex particles that have a central hydrophobic core of non-polar lipids, primarily cholesterol esters, and triglycerides. This hydrophobic core is surrounded by a hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins. Plasma lipoproteins are divided into seven classes based on size, lipid composition, and apolipoproteins.

Lipoprotein any member of a group of substances containing both lipid (fat) and protein. They occur in both soluble complexes as in egg yolk and mammalian blood plasma and insoluble ones, as in cell membranes. Lipoproteins in blood plasma have been intensively studied because they are the mode of transport for cholesterol through the bloodstream and lymphatic fluid.

• Chylomicrons – These are large triglyceride-rich particles made by the intestine, which are involved in the transport of dietary triglycerides and cholesterol to peripheral tissues and the liver. These particles contain apolipoproteins A-I, A-II, A-IV, A-V, B-48, C-II, C-III, and E. Apo B-48 is the core structural protein and each chylomicron particle contains one Apo B-48 molecule. The size of chylomicrons varies depending on the amount of fat ingested. A high-fat meal leads to the formation of large chylomicron particles due to the increased amount of triglyceride being transported whereas in the fasting state the chylomicron particles are small carrying decreased quantities of triglyceride.
• Chylomicron remnants – The removal of triglyceride from chylomicrons by peripheral tissues results in smaller particles called chylomicron remnants. Compared to chylomicrons these particles are enriched in cholesterol and are pro-atherogenic.
• Very low-density lipoproteins (VLDL) – These particles are produced by the liver and are triglyceride-rich. They contain apolipoprotein B-100, C-I, C-II, C-III, and E. Apo B-100 is the core structural protein and each VLDL particle contains one Apo B-100 molecule. Similar to chylomicrons the size of the VLDL particles can vary depending on the quantity of triglyceride carried in the particle. When triglyceride production in the liver is increased, the secreted VLDL particles are large. However, VLDL particles are smaller than chylomicrons.
• Intermediate density lipoproteins (IDL; VLDL remnants) – The removal of triglycerides from VLDL by muscle and adipose tissue results in the formation of IDL particles which are enriched in cholesterol. These particles contain apolipoprotein B-100 and E. These IDL particles are pro-atherogenic.
• Low-density lipoproteins (LDL) – These particles are derived from VLDL and IDL particles and they are even further enriched in cholesterol. LDL carries the majority of the cholesterol that is in the circulation. The predominant apolipoprotein is B-100 and each LDL particle contains one Apo B-100 molecule. LDL consists of a spectrum of particles varying in size and density. An abundance of small dense LDL particles are seen in association with hypertriglyceridemia, low HDL levels, obesity, type 2 diabetes (i.e. patients with metabolic syndrome), and infectious and inflammatory states. These small dense LDL particles are considered to be more pro-atherogenic than large LDL particles for a number of reasons. Small dense LDL particles have a decreased affinity for the LDL receptor resulting in a prolonged retention time in the circulation. Additionally, they more easily enter the arterial wall and bind more avidly to intra-arterial proteoglycans, which traps them in the arterial wall. Finally, small dense LDL particles are more susceptible to oxidation, which could result in an enhanced uptake by macrophages.
• High-density lipoproteins (HDL) – These particles play an important role in reverse cholesterol transport from peripheral tissues to the liver, which is one potential mechanism by which HDL may be anti-atherogenic. In addition, HDL particles have anti-oxidant, anti-inflammatory, anti-thrombotic, and anti-apoptotic properties, which may also contribute to their ability to inhibit atherosclerosis. HDL particles are enriched in cholesterol and phospholipids. Apolipoproteins A-I, A-II, A-IV, C-I, C-II, C-III, and E are associated with these particles. Apo A-I is the core structural protein and each HDL particle may contain multiple Apo A-I molecules. HDL particles are very heterogeneous and can be classified based on density, size, charge, or apolipoprotein composition.

 Lipoprotein

APOLIPOPROTEINS

Apolipoproteins have four major functions including 1) serving a structural role, 2) acting as ligands for lipoprotein receptors, 3) guiding the formation of lipoproteins, and 4) serving as activators or inhibitors of enzymes involved in the metabolism of lipoproteins (Table 3). Apolipoproteins thus play a crucial role in lipoprotein metabolism.

• Apolipoprotein A-I – Apo A-I is synthesized in the liver and intestine and is the major structural protein of HDL accounting for approximately 70% of HDL protein. It also plays a role in the interaction of HDL with ATP-binding cassette protein A1 (ABCA1), ABCG1, and class B, type I scavenger receptor (SR-B1). Apo A-I is an activator of lecithin: cholesterol acyltransferase (LCAT), an enzyme that converts free cholesterol into cholesteryl ester.
• Apolipoprotein A-II – Apo A-II is synthesized in the liver and is the second most abundant protein on HDL accounting for approximately 20% of HDL protein.
• Apolipoprotein A-IV (2) – Apo A-IV is synthesized in the intestine during fat absorption. Apo A-IV is associated with chylomicrons and high-density lipoproteins but is also found in the lipoprotein-free fraction. Its precise role in lipoprotein metabolism remains to be determined but studies have suggested a role for Apo A-IV in regulating food intake.
• Apolipoprotein A-V (3) – Apo A-V is synthesized in the liver and associates with triglyceride-rich lipoproteins. It is an activator of LPL mediated lipolysis and thereby plays an important role in the metabolism of triglyceride-rich lipoproteins.
• Apolipoprotein B-48 – Apo B-48 is synthesized in the intestine and is the major structural protein of chylomicrons and chylomicron remnants. There is a single molecule of apo B-48 per chylomicron particle. There is a single apolipoprotein B gene that is expressed in both the liver and intestine. The intestine expresses a protein that is approximately ½ the size of the liver due to mRNA editing. The aerobic-1 editing complex is expressed in the intestine and edits a specific cytidine to a uracil in the apo B mRNA in the intestine creating a stop codon that results in the cessation of protein translation and a shorter Apo B (Apo B-48). Notably, Apo B-48 is not recognized by the LDL receptor.
• Apolipoprotein B-100 – Apo B-100 is synthesized in the liver and is the major structural component of VLDL, IDL, and LDL. There is a single molecule of Apo B-100 per VLDL, IDL, and LDL particle. Apo B-100 is a ligand for the LDL receptor and therefore plays an important role in the clearance of lipoprotein particles.
• Apolipoprotein C – The C apolipoproteins are synthesized primarily in the liver and freely exchange between lipoprotein particles and therefore are found in association with chylomicrons, VLDL, and HDL.
• Apo C-II – is a co-factor for lipoprotein lipase (LPL) and thus stimulates triglyceride hydrolysis (4). Loss of function mutations in Apo C-II results in marked hypertriglyceridemia due to a failure to metabolize triglyceride-rich lipoproteins.
• Apo C-III is an inhibitor of LPL (5) – Additionally, Apo C-III inhibits the interaction of triglyceride-rich lipoproteins with their receptors. Recent studies have shown that loss of function mutations in Apo C-III lead to decreases in serum triglyceride levels and a reduced risk of cardiovascular disease. Interestingly, inhibition of Apo C-III expression results in a decrease in serum triglyceride levels even in patients deficient in lipoprotein lipase indicating that the ability of Apo C-III to modulate serum triglyceride levels is not dependent solely on regulating lipoprotein lipase activity.
• Apolipoprotein E (6) – Apolipoprotein E is synthesized in many tissues but the liver and intestine are the primary sources of circulating Apo E. Apo E exchanges between lipoprotein particles and is associated with chylomicrons, chylomicron remnants, VLDL, IDL, and a subgroup of HDL particles. There are three common genetic variants of Apo E (Apo E2, E3, and E4). ApoE2 differs from the most common isoform, Apo E3, by a single amino acid substitution where cysteine substitutes for arginine at residue 158. Apo E4 differs from Apo E3 at residue 112, where arginine substitutes for cysteine. Apo E3 and E4 are ligands for the LDL receptor while Apo E2 is poorly recognized by the LDL receptor. Patients who are homozygous for Apo E2 can develop familial dysbetalipoproteinemia. Apo E4 is associated with an increased risk of Alzheimer’s disease and an increased risk of atherosclerosis.
• Apolipoprotein (a) (7) – Apo (a) is synthesized in the liver. This protein is a homolog of plasminogen and its molecular weight varies from 300,000 to 800,000. It is attached to Apo B-100 via a disulfide bond. High levels of Apo (a) are associated with an increased risk of atherosclerosis. Apo (a) is an inhibitor of fibrinolysis and can also enhance the uptake of lipoproteins by macrophages, both of which could increase the risk of atherosclerosis. The physiologic function of Apo (a) is unknown. Interestingly this apolipoprotein is found in primates but not in other species.

LIPOPROTEIN RECEPTORS AND LIPID TRANSPORTERS

There are several receptors and transporters that play a crucial role in lipoprotein metabolism.

• LDL receptor (8) – The LDL receptor is present in the liver and most other tissues. It recognizes Apo B-100 and Apo E and hence mediates the uptake of LDL, chylomicron remnants, and IDL, which occurs via endocytosis. After internalization, the lipoprotein particle is degraded in lysosomes and the cholesterol is released. The delivery of cholesterol to the cell decreases the activity of HMGCoA reductase, a key enzyme in the biosynthesis of cholesterol, and the expression of LDL receptors. LDL receptors in the liver play a major role in determining plasma LDL levels (a low number of receptors is associated with high plasma LDL levels while a high number of hepatic LDL receptors is associated with low plasma LDL levels). The number of LDL receptors is regulated by the cholesterol content of the cell. When cellular cholesterol levels are decreased the transcription factor SREBP is transported from the endoplasmic reticulum to the Golgi where proteases cleave and activate SREBP, which then migrates to the nucleus and stimulates the expression of LDL receptors (Figure 4). Conversely, when cellular cholesterol levels are high SREBP remains in the endoplasmic reticulum in an inactive form and the expression of LDL receptors is low.
• LDL receptor-related protein (LRP) (10) – LRP is a member of the LDL receptor family. It is expressed in multiple tissues including the liver. LRP recognizes Apo E and mediates the uptake of chylomicron remnants and IDL.
• Class B scavenger receptor B1 (SR-B1) (11) – SR-B1 is expressed in the liver, adrenal glands, ovaries, testes, macrophages, and other cells. In the liver and steroid producing cells, it mediates the selective uptake of cholesterol esters from HDL particles. In macrophages and other cells, it facilitates the efflux of cholesterol from the cell to HDL particles.
• ATP-binding cassette transporter A1 (ABCA1) (12) – ABCA1 is expressed in many cells including hepatocytes, enterocytes, and macrophages. It mediates the transport of cholesterol and phospholipids from the cell to lipid poor HDL particles (pre-beta-HDL).
• ATP-binding cassette transporter G1 (ABCG1) (13) – ABCG1 is expressed in many different cell types and mediates the efflux of cholesterol from the cell to HDL particles.
• ATP-binding cassette transporter G5 and G8 (ABCG5/ABCG8) (14) – ABCG5 and ABCG8 are expressed in the liver and intestine and form a heterodimer. In the intestine, these transporters mediate the movement of plant sterols and cholesterol from inside the enterocyte into the intestinal lumen thereby decreasing their absorption and limiting the uptake of dietary plant sterols. In the liver, these transporters play a role in the movement of cholesterol and plant sterols into the bile facilitating the excretion of plant sterols.
• Niemann-Pick C1-Like 1 (NPC1L1) (14) – NPC1L1 is expressed in the intestine and mediates the uptake of cholesterol and plant sterols from the intestinal lumen into the enterocyte.

ENZYMES AND TRANSFER PROTEINS INVOLVED IN LIPOPROTEIN METABOLISM

There are several enzymes and transfer proteins that play a key role in lipoprotein metabolism.

• Lipoprotein lipase (LPL) (15) – LPL is synthesized in muscle, heart, and adipose tissue, then secreted and attached to the endothelium of the adjacent blood capillaries. This enzyme hydrolyzes the triglycerides carried in chylomicrons and VLDL to fatty acids, which can be taken up by cells. The catabolism of triglycerides results in the conversion of chylomicrons into chylomicron remnants and VLDL into IDL. This enzyme requires Apo C-II as a cofactor. Apo A-V also plays a key role in the activation of this enzyme. In contrast, Apo C-III and Apo A-II inhibit the activity of LPL. Insulin stimulates LPL expression and LPL activity is reduced in patients with poorly controlled diabetes, which can impair the metabolism of triglyceride-rich lipoproteins leading to hypertriglyceridemia.
• Hepatic lipase (16) – Hepatic lipase is localized to the sinusoidal surface of liver cells. It mediates the hydrolysis of triglycerides and phospholipids in IDL and LDL leading to smaller particles (IDL is converted to LDL; LDL is converted from large LDL to small LDL). It also mediates the hydrolysis of triglycerides and phospholipids in HDL resulting in smaller HDL particles.
• Endothelial lipase (17) – This lipase plays a major role in hydrolyzing the phospholipids in HDL.
• Lecithin – cholesterol acyltransferase (LCAT) (18) LCAT is made in the liver. In the plasma, it catalyzes the synthesis of cholesterol esters in HDL by facilitating the transfer of fatty acid from position 2 of lecithin to cholesterol. This allows for the transfer of the cholesterol from the surface of the HDL particle (free cholesterol) to the core of the HDL particle (cholesterol ester), which facilitates the continued uptake of free cholesterol by HDL particles by reducing the concentration of cholesterol on the surface of HDL.
• Cholesteryl ester transfer protein (CETP) (19) – This protein is synthesized in the liver and in the plasma mediates the transfer of cholesterol esters from HDL to VLDL, chylomicrons, and LDL and the transfer of triglycerides from VLDL and chylomicrons to HDL. Inhibition of CETP activity leads to an increase in HDL cholesterol and a decrease in LDL cholesterol.

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• https://www.ncbi.nlm.nih.gov/books/NBK459188/
• https://www.ncbi.nlm.nih.gov/books/NBK545157/
• https://en.wikipedia.org/wiki/Lipoprotein
• https://medlineplus.gov/hdlthegoodcholesterol.html
• https://www.fda.gov/food/food-labeling-nutrition/changes-nutrition-facts-label
• https://www.cdc.gov/cholesterol/facts.htm
• https://www.nhlbi.nih.gov/health-topics/publications-and-resources
• https://en.wikipedia.org/wiki/High-density_lipoprotein
• https://www.sciencedirect.com/topics/medicine-and-dentistry/high-density-lipoprotein
• https://www.heart.org/en/health-topics/cholesterol/hdl-good-ldl-bad-cholesterol-and-triglycerides

Elbow arthrocentesis is a procedure performed to aspirate the contents of a joint cavity to evaluate and treat elbow effusion. Arthrocentesis is considered a minor surgical procedure. However, there is always the chance, as with introducing any needle through the skin, for infection, injury to nerves, vessels, tendons, or other connective tissue. Therefore, this procedure should only be performed by health care providers trained in arthrocentesis with a strong understanding of elbow anatomy. Arthrocentesis is commonly used to evaluate the underlying etiology of joint effusion, including infectious, inflammatory, and hemorrhagic causes. Aspiration of the joint space and removal of the contents reduces the fluid pressure in the joint capsule and reduces pain. Additionally, access to the joint space provides the opportunity to inject therapeutic agents in the setting of pain or degenerative joint disease. Of the etiologies above, the most important to diagnose properly is septic arthritis, as cultures are crucial to prompt and adequate treatment.

Anatomy and Physiology

• Osseous – The distal humerus, radial head, and olecranon comprise the elbow joint.  The olecranon process articulates with the trochlea of the humeral condyle forming a hinge joint for flexion and extension.  The radial head is held in place with the annular ligament arising from the proximal ulna and articulates with the ulna and the distal humerus.  The joint is encapsulated and contains the articular surfaces of the structures mentioned above. This space contains synovial fluid and is the target of elbow aspiration.
• Muscular Compartments – The biceps crosses the elbow anteriorly, and the triceps crosses the elbow posteriorly, facilitating flexion and extension, respectively.  The flexor carpi radialis, palmaris longus, humeroulnar head of flexor digitorum superficials, and the humeral head of the flexor carpi ulnaris contribute to the flexor compartment and supination of the wrist originating at the medial epicondyle.  They primarily receive innervation via the median nerve.  The wrist extensors and supinators, including extensor carpi radialis brevis, extensor digitorum, and extensor digiti minimi, all originate on the lateral epicondyle and are innervated by the radial nerve.
• Vasculature – Blood supply to the elbow is via extensive anastomoses originating from the brachial and radial arteries
• Positioning – The patient should have their elbow bent to 90 degrees with their hand pronated (palm down); this exposes the approach trajectory by rolling the head of the radius out of the way. The aiming point for needle insertion is the juncture of the lateral humeral condyle, radial head, and olecranon process. These three landmarks form the anconeus triangle, and the insertion point is located centrally.  The needle is then inserted into the sulcus directed medial and perpendicular to the radius toward the distal end of the antecubital fossa.

Ultrasound guidance for the evaluation of fluid collection and needle guidance is recommended.

Indications of Elbow Arthrocentesis

• Elbow arthrocentesis is performed to aspirate effusions for two reasons, both diagnosis and therapeutic relief of pain caused by fluid pressure.
• Diagnostically the primary etiologies of concern are septic arthritis, hemarthrosis, and inflammation. Of these, a suspected septic joint and crystalline arthropathy are the two most common indications.
• Additionally, arthrocentesis may help to evaluate the therapeutic response for septic arthritis or unexplained arthritis with synovial effusion.
• Although not the topic of this discussion, access to the joint space may also be used to inject therapeutic agents and to challenge the joint with fluid for evaluation of joint capsule integrity if any overlying laceration is present.[rx]

Contraindications of Elbow Arthrocentesis

The only absolute contraindication to arthrocentesis is overlying cellulitis, which may lead to the seeding of the joint with bacteria.[rx] Relative contraindications include coagulopathy, joint prosthesis, acute fracture, and adjacent osteomyelitis. Prosthetic joints warrant discussion with orthopedic surgery before tapping, as many surgeons believe a prosthetic joint should only undergo tapping in the operative theater.

Equipment

• Iodine solution or chlorhexidine
• Sterile gloves and drape
• Sterile gauze
• Sterile fenestrated drapes
• Lure-Lok syringes including one 5cc and another 5 to 20cc syringe
• 20G and 27G needle
• 1% Lidocaine or 0.5% bupivacaine
• Collection tubes including a hematology tube, sterile tube, heparinized tube
• Ultrasound with a sterile cover, if available

Personnel

This procedure can take place without an assistant; however, an assistant may make certain situations, including an anxious patient or unforeseen technical difficulties, easier.

Preparation

There are no stat indications for elbow arthrocentesis; thus, additional time can help improve a first-attempt success rate and reduce associated risks. Ensure all necessary equipment is available and works appropriately, correctly identify landmarks, and adhere to a sterile technique.

Technique

Position your patient with the elbow bent 90 degrees and pronated palm down. This position rolls the radial head to open the joint space. Use an ultrasound if available to localize fluid collection and direct the needle. Mark the approach by identifying the insertion site inferior to the lateral humeral epicondyle, anterior to the olecranon, and superior/posterior to the radial head (anconeus triangle). Use a skin pen to mark or pressure to indent the surface of the skin. Now clean the area with a wide margin using chlorhexidine or iodine solution. Gown, glove, and then drape in a sterile fashion. Raise a bleb of 1% lidocaine using a sterile technique at the site of insertion. Once anesthetized, an 18 to 22 gauge needle 1.5 inches long is attached to a 5 to 10mL syringe and advanced into the joint space while retracting to watch for blood return. Once the joint space is accessed, synovial fluid, blood, or infectious material may be aspirated. With the needle held in place, multiple syringes may be used to aspirate all the contents of the joint. If inflammatory etiology is suspected, a glucocorticoid may be injected before leaving the joint space to prevent relapse of effusion.[rx] The needle is then withdrawn, a bandage is applied, and the collected fluid is sent to the lab. Studies should include fluid gram stain and culture, cell count with differential, protein, glucose, and polarized light microscopy for crystalline arthropathies.[rx][rx][rx]

Other Considerations – Joint aspiration is safe within the therapeutic range of anticoagulation with warfarin or properly dosed DOC.  Considerations for the anticoagulated patient includes using a smaller needle size.[rx][rx][rx] Ultrasonography may be used in a sterile fashion to guide the needle if a dry tap occurs, and septic arthritis is suspected.[rx] Shaving is of no benefit.

Complications

Even though complications with arthrocentesis are rare, the clinician should take the time to inform the patient of potential complications arising from arthrocentesis. There are two major categories to take into consideration; infectious complications and noninfectious complications. Of the complications, the most feared is septic arthritis.[rx]  The frequency of this complication lies somewhere between 1 in 2000 and 1 in 15000. It is best avoided by maintaining a sterile field, minimizing attempts, using single-dose vials, changing to a new needle after drawing up medication before injecting, and preventing the introduction of a needle through cellulitis. The other concerning infection is septic bursitis, which arises when the needle approach travels through a bursa, the olecranon bursa in the case of the elbow, on the way to the joint and is due to direct inoculation from skin flora. Noninfectious complications that arise include tendon rupture, vascular damage, and neurologic damage. All three complications directly result from trauma secondary to the penetrating needle and are more common when injecting glucocorticoids than aspirating. These complications are mediated by carefully planning the approach and identifying the proper anatomical location for insertion and needle travel.  Bleeding management is with tamponade. The patient should also be informed there may be a recurrence of joint effusion until the resolution of the underlying etiology.[rx]

• https://www.ncbi.nlm.nih.gov/books/NBK532279/
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• https://www.ncbi.nlm.nih.gov/books/NBK518967/
• https://en.wikipedia.org/wiki/Synovial_fluid

Hearing loss is an extremely common medical condition, progressing in incidence and severity with age. The affected population is also vast, varying between neonates to elderly patients, and is nearly omnipresent in the 70+ age group.[rx] The diagnosis and management require a multi-disciplinary team that includes the general practitioner, otolaryngologist, speech therapist, audiologist, and social worker. To correctly address hearing loss, understanding the nature of hearing loss, and the equipment that is needed to improve auditory reception is crucial. In terms of children’s hearing loss, pediatricians need to be integrated into their care to ensure the normal hearing and language development of the child.[rx][rx]

Hearing loss is a partial or total inability to hear.^[rx] Hearing loss may be present at birth or acquired at any time afterward.^[rx][rx] Hearing loss may occur in one or both ears.^[rx] In children, hearing problems can affect the ability to learn spoken language, and in adults, it can create difficulties with social interaction and at work.^[rx] Hearing loss can be temporary or permanent. Hearing loss related to age usually affects both ears and is due to cochlear hair cell loss.^[rx] In some people, particularly older people, hearing loss can result in loneliness.^[rx] Deaf people usually have little to no hearing.^[rx]

Types of Hearing Loss

• Sudden sensorineural hearing loss (SSHL) – presumed to be of viral origin, is an otologic emergency that is medically treated with corticosteroids.
• Sensorineural hearing loss – can occur from head trauma or abrupt changes in air pressure (e.g., airplane descent), which can cause inner ear fluid compartment rupture or leakage, which can be toxic to the inner ear. There has been a variable success with emergency surgery when this happens.
• Bilateral progressive hearing loss – over several months, also diagnosed as autoimmune inner ear disease, is managed medically with long-term corticosteroids and sometimes with drug therapy. Autoimmune inner ear disease is when the body’s immune system misdirects its defenses against the inner ear structures to cause damage in this part of the body.
• Fluctuating sensorineural hearing loss – may be from an unknown cause or associated with Ménière’s disease. Symptoms of Meniere’s disease are hearing loss, tinnitus (ringing in the ears), and vertigo. Ménière’s disease may be treated medically with a low-sodium diet, diuretics, and corticosteroids. If the vertigo is not medically controlled, then various surgical procedures are used to eliminate vertigo.
• Sensorineural hearing loss from disease – in the central nervous system may respond to medical management for the specific disease affecting the nervous system. For example, hearing loss secondary to multiple sclerosis may be reversed with treatment for multiple sclerosis.
• Irreversible sensorineural hearing loss – the most common form of hearing loss, maybe managed with hearing aids. When hearing aids are not enough, this type of hearing loss can be surgically treated with cochlear implants.

There are four levels of deafness or hearing impairment. These are

• Mild deafness or mild hearing impairment – The person can only detect sounds between 25 and 29 decibels (dB). They may find it hard to understand the words other people are saying, especially if there is a lot of background noise.
• Moderate deafness or moderate hearing impairment – The person can only detect sounds between 40 and 69 dB. Following a conversation using hearing alone is very difficult without using a hearing aid.
• Severe deafness – The person only hears sounds above 70 to 89 dB. A severely deaf person must either lip-read or use sign language in order to communicate, even if they have a hearing aid.
• Profound deafness – Anybody who cannot hear a sound below 90dB has profound deafness. Some people with profound deafness cannot hear anything at all, at any decibel level. Communication is carried out using sign language, lip-reading, or reading and writing.

Causes of Hearing Loss

The normal hearing function involves sound waves arriving at the auricle, passing through the external auditory canal (EAC), causing a vibration of the tympanic membrane [rx]. Vibration then gets transmitted via the ossicles (malleus, incus, stapes) to the cochlea. Subsequently, hair cells inside the cochlea stimulate the eighth cranial nerve that transfers the stimuli to the brain. Processing of crude sounds occurs in the higher cortices of the brain and this includes the comprehension of language.

Hearing loss can be conductive, sensorineural, or mixed.[rx] Conductive hearing loss takes place with disruption of the transmission of the sound waves to the cochlea. The most common causes include abnormal formation of the auricle or helix, cerumen impaction, ear canal foreign bodies, otitis externa, dysfunction or fixation of the ossicular chain, and middle ear effusion. Cholesteatoma, a benign though locally-destructive trapping of squamous debris arising from the tympanic membrane, as well as other benign or malignant tumors, can result in conductive hearing loss.

Sensorineural hearing loss (SNHL) usually results from problematic transmission of the stimuli at or after the cochlea.[rx] This loss could be related to hair cell dysfunction or a disorder of the eighth nerve itself. The main difference between the two kinds of hearing loss, apart from the pathophysiological features, is that patients with conductive hearing loss perceive the sounds diminished, while SNHL patients may perceive the sounds diminished and distorted.

Hearing loss that involves problematic transmission before and after the cochlea is called mixed hearing loss.

There are multiple reasons for hearing impairment. In the pediatric population, genetic causes are the most common, accounting for more than 50% of hearing loss. Genetic causes involve various syndromes that have hearing loss as one of their features; however, there is an entire entity of non-syndromic genetic hearing loss, wherein patients suffer hearing loss while the rest of their function is normal.[rx] Mutations, autosomal differences, as well as unknown genetic diversity, relates to this type of hearing loss.[rx] Prenatal causes can also relate to hearing loss in infants. These include exposure to various bacterial or viral infections as well as different teratogens. Perinatal causes are less common, predominantly related to prematurity, low APGAR score, neonatal jaundice, and sepsis.[rx] Postnatal causes such as meningococcal infections and mumps can also cause hearing loss as a late complication, as well as head injuries or chronic or recurrent otitis media.[rx]

Age-related hearing loss involves a gradual reduction of hearing capacity of the individual and poor speech discrimination scores, most noticeable initially in noisy environments, which is likely related to age-related degeneration of the cochlea in various sites, particularly the hair cells.[rx] Otosclerosis and cholesteatomas are leading causes of conductive hearing loss.[rx] Another entity that can occur in the adult population is sudden sensorineural hearing loss.[rx] This condition is very specific, with a sudden or rapid onset of hearing loss in one ear. This is often preceded by a viral upper respiratory infection, and virally-mediated inflammatory markers are the presumed cause.[rx]

Hearing loss can be broadly characterized as congenital or acquired in the pediatric population.

Congenital causes may lead to hearing loss being present or acquired soon after birth. Hearing loss can be caused by hereditary and non-hereditary genetic factors or by certain complications during pregnancy and childbirth, including:

• maternal rubella, syphilis, or certain other infections during pregnancy;
• low birth weight;
• birth asphyxia (a lack of oxygen at the time of birth);
• inappropriate use of particular drugs during pregnancy, such as aminoglycosides, cytotoxic drugs, antimalarial drugs, and diuretics;
• severe jaundice in the neonatal period, which can damage the hearing nerve in a newborn infant.

Acquired causes

Acquired causes may lead to hearing loss at any age, such as:

• infectious diseases including meningitis, measles and mumps;
• chronic ear infections;
• collection of fluid in the ear (otitis media);
• use of certain medicines, such as those used in the treatment of neonatal infections, malaria, drug-resistant tuberculosis, and cancers;
• injury to the head or ear;
• excessive noise, including occupational noise such as that from machinery and explosions;
• recreational exposure to loud sounds such as that from use of personal audio devices at high volumes and for prolonged periods of time and regular attendance at concerts, nightclubs, bars and sporting events;
• ageing, in particular due to degeneration of sensory cells; and
• wax or foreign bodies blocking the ear canal.

Among children, chronic otitis media is a common cause of hearing loss.

High-risk factors in neonates

• Damage to the inner ear – Aging and exposure to loud noise may cause wear and tear on the hairs or nerve cells in the cochlea that send sound signals to the brain. When these hairs or nerve cells are damaged or missing, electrical signals aren’t transmitted as efficiently, and hearing loss occurs. Higher pitched tones may become muffled to you. It may become difficult for you to pick out words against background noise.
• The gradual buildup of earwax – Earwax can block the ear canal and prevent conduction of sound waves. Earwax removal can help restore your hearing.
• Ear infection and abnormal bone growths or tumors – In the outer or middle ear, any of these can cause hearing loss.
• Ruptured eardrum (tympanic membrane perforation) – Loud blasts of noise, sudden changes in pressure, poking your eardrum with an object and infection can cause your eardrum to rupture and affect your hearing.
• Congenital infections
• Family history
• Craniofacial anomalies
• Hyperbilirubinemia
• Birth weight 1500 g
• Low Apgar
• Bacterial meningitis
• Need to prolonged intubation
• chickenpox
• cytomegalovirus
• mumps
• meningitis
• sickle cell disease
• syphilis
• lyme disease
• diabetes
• hypothyroidism
• arthritis
• some cancers
• teenagers exposed to second-hand smoke

Symptoms of Hearing Loss

Signs and symptoms of hearing loss may include:

• Muffling of speech and other sounds
• Difficulty understanding words, especially against background noise or in a crowd
• Trouble hearing consonants
• Frequently asking others to speak more slowly, clearly and loudly
• Needing to turn up the volume of the television or radio
• Withdrawal from conversations
• Avoidance of some social settings
• difficulty using the telephone
• loss of sound localization
• difficulty understanding speech, especially of children and women whose voices are of a higher frequency.
• difficulty understanding speech in the presence of background noise (cocktail party effect)
• sounds or speech sounding dull, muffled or attenuated
• need for increased volume on television, radio, music and other audio sources
• pain or pressure in the ears
• a blocked feeling
• hyperacusis, heightened sensitivity with accompanying auditory pain to certain intensities and frequencies of sound, sometimes defined as “auditory recruitment”
• tinnitus, ringing, buzzing, hissing or other sounds in the ear when no external sound is present
• vertigo and disequilibrium
• trypanophobia, also known as Euphonia, abnormal hearing of one’s own voice and respiratory sounds, usually as a result of a patulous (a constantly open) eustachian tube or dehiscent superior semicircular canals
• disturbances of facial movement (indicating a possible tumor or stroke) or in persons with Bell’s Palsy

Hearing impairment in infants

The following signs may indicate a hearing problem:

• Before the age of 4 months, the baby does not turn their head toward a noise.
• By the age of 12 months, the baby still has not uttered a single word.
• The infant does not appear to be startled by a loud noise.
• The infant responds to you when they can see you, but respond far less or do not respond at all when you are out of sight and call out their name.
• The infant only seems to be aware of certain sounds.

Hearing impairment in toddlers and children

These signs might become more evident in slightly older children:

• The child is behind others the same age in oral communication.
• The child keeps saying “What?” or “Pardon?”
• The child talks in a very loud voice, and tends to produce louder-than-normal noises.
• When the child speaks, their utterances are not clear.

Diagnosis of Hearing Loss

History and Physical

History in pediatric cases is critical for early diagnosis of hearing loss. This history involves questions regarding the prenatal history of the child, their delivery, and the first days of life as well as the post-natal history up until the moment of the symptom presentation, as well as a family history of hearing loss. A child with hearing loss may present with non-reaction to sounds, behavioral problems, speech issues, language delay, or even school failure, as well as mispronouncing words. Family history, especially if there is a member with early hearing loss, also has great value in suspecting hearing loss.[rx]

Adult history acquisition is more straightforward and involves questions regarding the onset of symptoms, the severity, the presence of vertigo, neurological symptoms, infections, and other conditions that could be related to hearing loss. Past medical history, as well as family history, along with work and noise exposure, are also important. In this way, there is a differentiation between the causes of hearing loss, and the clinician can proceed to the appropriate investigations.[rx]

Physical examination involves a full otolaryngology examination, with otoscopy bilaterally (including pneumatic otoscopy) to rule out any obvious conductive hearing loss.[rx] Foreign bodies, cerumen, infections, tympanic membrane perforations, as well as middle ear effusion, need to be ruled out in the first instance. Subsequently, identification of dysmorphic and other physical findings is essential, especially in young children and infants. These can include facial abnormalities or asymmetry, ear, neck and skin anomalies, other organ dysfunction, or even balance irregularities. As a result, a comprehensive inspection, otoscopy, and neurological examination are crucial to reach the correct diagnosis. Weber and Rinne tests are easy, fast, and globally useful to differentiate between SNHL and conductive hearing loss and may aid in interpreting the formal audiogram.

Evaluation

An accurate hearing evaluation is possible for the population of all ages, though there are specific limitations that are age- or cognition-related regarding formal audiometric evaluation that may complicate the picture. According to the American Academy of Pediatrics as well as the Joint Committee on Infant Hearing, all infants should undergo a hearing evaluation to rule out any hearing impairment at birth, or by the age of one month.[rx] Additionally, all newborns and infants with hearing loss need to get a comprehensive evaluation that focuses on medical and birth history as well as a family history for the previous three generations according to the American College of Medical Genetics and Genomics.[rx]

Hearing loss evaluation can differ according to the age of the child. BAER (brainstem audio-evoked response) test is the method for early diagnosis of hearing loss in newborns and infants. Otoacoustic emissions are also an option in newborns, and it is an easy, inexpensive technique, but they are less reliable than BAER tests. Finally, audiometry works with older children, aged 4 to 5 and older, who can respond to sound stimuli according to instructions. There are age-specific audiometric tests that can be performed. Young, pre-lingual, children can be conditioned to respond to play stimuli that can assess whether they can hear. This method of testing is not ear-specific, and can only confirm they have at least one ear that can hear at a given test level. This is important because as long as there is one ear that hears at a normal level, normal language development can be expected. Tympanograms and audiograms are of value in adults and children, but provide information only regarding the mobility of the tympanic membrane.[rx]

General screening test

A doctor may ask the patient to cover one ear and describe how well they hear words spoken at different volumes, as well as checking sensitivity to other sounds. If the doctor suspects a hearing problem, they will probably be referred to either an ear, nose, and throat (ENT) specialist or an audiologist.

Further tests will be carried out, including:

• A tuning fork test – This is also known as the Rinne test. A tuning fork is a metal instrument with two prongs that produces a sound when it is struck. Simple tuning fork tests may help the doctor detect whether there is any hearing loss, and where the problem is. A tuning fork is vibrated and placed against the mastoid bone behind the ear. The patient is asked to indicate when they no longer hear any sound. The fork, which is still vibrating, is then placed 1 to 2 centimeters (cm) from the auditory canal. The patient is asked again whether they can hear the fork.
• Audiometer test – The patient wears earphones, and sounds are directed into one ear at a time. A range of sounds is presented to the patient at various tones. The patient has to signal each time a sound is heard. Each tone is presented at various volumes, so that the audiologist can determine at which point the sound at that tone is no longer detected. The same test is carried out with words. The audiologist presents words at various tones and decibel levels to determine where the ability to hear stops.
• Bone oscillator test – This is used to find out how well vibrations pass through the ossicles. A bone oscillator is placed against the mastoid. The aim is to gauge the function of the nerve that carries these signals to the brain.
• App-based hearing tests – Mobile apps are available that you can use by yourself on your tablet to screen for moderate hearing loss.
• Tuning fork tests – Tuning forks are two-pronged, metal instruments that produce sounds when struck. Simple tests with tuning forks can help your doctor detect hearing loss. This evaluation may also reveal where in your ear the damage has occurred.
• Audiometer tests – During these more-thorough tests conducted by an audiologist, you wear earphones and hear sounds and words directed to each ear. Each tone is repeated at faint levels to find the quietest sound you can hear.

Routine screening of children

The American Academy of Pediatrics (AAP) recommends that children have their hearing tests at the following times:

• when they start school
• at 6, 8, and 10 years of age
• at least once when they are in middle school
• once during high school

Testing newborns

The otoacoustic emissions (OAE) test involves inserting a small probe into the outer ear; it is usually done while the baby is asleep. The probe emits sounds and checks for “echo” sounds bouncing back from the ear. If there is no echo, the baby might not necessarily have a hearing problem, but doctors will need to carry out further tests to make sure and to find out why

Treatment of Hearing Loss

Management of conductive hearing loss focuses on the treatment of the underlying disease. Conservative methods such as removal of the foreign body, micro-suction of the cerumen or discharge in the ear canal are necessary if the ear canal is blocked [rx]. With regards to otitis media, myringotomy to release the middle ear fluid will allow the sound wave to reach the cochlea, while ventilation tubes are useful if the otitis media is persistent, causing hearing loss. However, evidence shows that hearing loss can represent a post-operative complication due to tympanosclerosis, though this is very rare.[rx] Finally, if the hearing loss is due to cholesteatoma, this requires surgical removal with results in hearing restoration dependent upon the degree of destruction of the middle ear structures. Chronic or refractory, inoperable, conductive hearing loss can be treated with bone-conduction hearing aids or via a BAHA, a bone-implanted conduction aid, with excellent results.[rx]

Conservative treatment of sensorineural hearing involves the use of assistive listening devices and amplification. Hearing aids are devices designed to improve audition up to 40 to 60 dB with good results. They require individualized fittings and venting plans and can be very expensive.  The overall results are very good.[rx] Surgical treatment is provided to infants diagnosed with SNHL, as they undergo cochlear implantation under the age of 6 months.[rx] The intervention requires an ear, nose, and throat specialist, and long-term monitoring is essential to ensure normal linguistic and social development of the child. Similarly, refractory, severe SNHL in adults can be treated with cochlear implantation. This will destroy any remnant native hearing, replacing it with the device, so this must be done judiciously. Excellent outcomes have been achieved routinely with this procedure in severe SNHL.

Staging

According to the American National Standards Institute, hearing loss ranking is as follows:

• Slight hearing loss: 16 to 25 dB
• Mild hearing loss: 26 to 40 dB
• Moderate hearing loss: 41 to 55 dB
• Severe hearing loss: 71 to 90 dB
• Profound: over 90 dB

Complications

Complications of hearing loss in children involve speech delay and failure to thrive in school. Any child with a speech delay requires a formal hearing evaluation, as this is the most common cause.

Adult patients, who are frequently elderly, can easily become isolated and depressed if their hearing loss is not addressed.[rx]

WHO response

WHO assists Members States in developing programs for ear and hearing care that are integrated into the primary health-care system of the country. WHO’s work includes:

• providing technical support to the Member States in the development and implementation of national plans for hearing care;
• providing technical resources and guidance for training of health-care workers on hearing care;
• developing and disseminating recommendations to address the major preventable causes of hearing loss;
• undertaking advocacy to raise awareness about the prevalence, causes, and impact of hearing loss as well as opportunities for prevention, identification, and management;
• developing and disseminating evidence-based tools for effective advocacy;
• observing and promoting World Hearing Day as an annual advocacy event;
• building partnerships to develop strong hearing care programmes, including initiatives for affordable hearing aids, cochlear implants and services;
• collating data on deafness and hearing loss to demonstrate the scale and the impact of the problem;
• launching and promoting the WHO-ITU global standard for personal audio systems and devices;
• promoting safe listening to reduce the risk of recreational noise-induced hearing loss through the WHO Make Listening Safe initiative;
• raising awareness on safe listening to reduce the risk of recreational noise-induced hearing loss through the WHO Make Listening Safe initiative;
• promoting the social inclusion of people with disabilities, including people with hearing loss and deafness, for example, through community-based rehabilitation networks and programs.
• launching and hosting the World Hearing Forum, which is a global advocacy alliance of all stakeholders in the field of hearing.
• In 2017, the 70^th World Health Assembly adopted a resolution on the prevention of deafness and hearing loss. This resolution calls upon the Member States to integrate strategies for ear and hearing care within the framework of their primary health care systems, under the umbrella of universal health coverage. It also requests WHO to undertake a number of actions for the promotion of ear and hearing care at the global level, including many of those noted above.

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Enlarge Spleen/Splenomegaly is defined as enlargement of the spleen measured by weight or size. The spleen plays a significant role in hematopoiesis and immunosurveillance. The major functions of the spleen include clearance of senescent and abnormal erythrocytes and their remnants, opsonized platelets and white blood cells and removal of microorganisms and antigens. The spleen also serves as a secondary lymphoid organ and is the site for maturation and storage of T and B lymphocytes, playing an important role in the synthesis of immunoglobulin G (IgG) by mature B-lymphocytes upon interaction with the T-lymphocytes.  The spleen also synthesizes the immune system peptides properdin and tuftsin. Approximately one-third of circulating platelets are stored in the spleen. The normal position of the spleen is within the peritoneal cavity in the left upper quadrant adjacent to ribs 9 through 12. The normal-sized spleen abuts the stomach, colon, and left kidney.

The size and weight of spleen may vary and correlates with weight, height, and sex of an individual, with larger spleen size seen in men compared to women, and in heavier or taller individuals. A normally sized spleen measures up to 12 cm in craniocaudal length.  A length of 12 cm to 20 cm indicates splenomegaly, and a length greater than 20 cm is definitive of massive splenomegaly. The normal weight of the adult spleen is 70 g to 200 g; a spleen weight of 400 g to 500 g indicates splenomegaly and a spleen weight greater than 1000 g is definitive of massive splenomegaly. The normal-sized spleen is usually not palpable in adults. However, it may be palpable due to variations in body habitus and chest wall anatomy. Splenomegaly may be diagnosed clinically or radiographically using ultrasound, CT imaging, or MRI.  Splenomegaly may be a transient condition due to acute illness or may be due to serious underlying acute or chronic pathology.[rx][rx][rx]

Splenomegaly is an enlargement of the spleen.^[rx] The spleen usually lies in the left upper quadrant (LUQ) of the human abdomen. Splenomegaly is one of the four cardinal signs of hypersplenism which include: some reduction in the number of circulating blood cells affecting granulocytes, erythrocytes, or platelets in any combination; a compensatory proliferative response in the bone marrow; and the potential for correction of these abnormalities by splenectomy. Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a response to hyperfunction. It is therefore not surprising that splenomegaly is associated with any disease process that involves abnormal red blood cells being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by leukemias and lymphomas. Thus, the finding of an enlarged spleen, along with caput-medusae, is an important sign of portal hypertension.^[rx]

Types of Enlarge Spleen

Splenomegaly can be classified based on its pathophysiologic mechanism:

• Congestive – by pooled blood (e.g., portal hypertension)
• Infiltrative – by invasion by cells foreign to the splenic environment (e.g., metastases, myeloid neoplasms, lipid storage diseases)
• Immune – by an increase in immunologic activity and subsequent hyperplasia (e.g., endocarditis, sarcoidosis, rheumatoid arthritis)
• Neoplastic – when resident immune cells originate a neoplasm (e.g., lymphoma).

The standard system for classifying splenomegaly on radiography is:^[rx][rx]

• Normal (not splenomegaly) – the largest dimension is less than 11 cm
• Moderate splenomegaly – the largest dimension is between 11–20 cm
• Severe splenomegaly – the largest dimension is greater than 20 cm

Causes of Enlarge Spleen

There are several potential causes of splenomegaly.

• Liver disease (cirrhosis, hepatitis): Parenchymal liver disease causes increased vascular pressure leading to an increase in spleen size.
• Hematologic malignancies (lymphomas, leukemias, myeloproliferative disorders): Neoplastic cells cause infiltration of the spleen leading to splenomegaly.
• Venous thrombosis (portal or hepatic vein thrombosis): This leads to an increase in vascular pressure leading to splenomegaly.
• Splenic congestion (venous thrombosis, portal hypertension, congestive heart failure).
• Cytopenias (Immune thrombocytopenic purpura, autoimmune hemolytic anemia, immune-mediated neutropenia, Felty syndrome): Immune-mediated destruction of red blood cells, white blood cells or platelets lead to functional splenomegaly.
• Splenic sequestration (pediatric sickle cell disease, hemolytic anemias, thalassemias).
• Acute or chronic infection (bacterial endocarditis, infectious mononucleosis, HIV, malaria, tuberculosis, histiocytosis, abscess).
• Connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis, Adult-onset Still’s disease, and some familial autoinflammatory syndromes).[rx][rx]
• Infiltrative disorders (sarcoidosis, amyloidosis, glycogen storage diseases).
• Splenic sequestration (pediatric sickle cell, hemolytic anemias, thalassemias).
• Focal lesions (hemangiomas, abscess, cysts, metastasis).
• malaria
• Hodgkin’s disease
• leukemia
• heart failure
• cirrhosis
• tumors in the spleen or from other organs that have spread to the spleen
• viral, bacterial, or parasitic infections
• inflammatory diseases, such as lupus or rheumatoid arthritis
• sickle cell disease

The mechanism underlying splenic enlargement varies based on the etiology. In the case of acute infectious illness, the spleen performs increased work in clearing antigens and producing antibodies and increases the number of reticuloendothelial cells contained within the spleen. These increased immune functions may result in splenic hyperplasia. In the case of liver disease and congestion, underlying illness causes increased venous pressure causing congestive splenomegaly. Extramedullary hematopoiesis exhibited in myeloproliferative disorders can lead to splenic enlargement (infiltrative splenomegaly).[rx][rx]

The possible causes of moderate splenomegaly (spleen <1000 g) are many and include

The causes of massive splenomegaly (spleen >1000 g) are

• chronic myelogenous leukemia
• myelofibrosis
• malaria
• Inflammatory diseases such as sarcoidosis, lupus, and rheumatoid arthritis
• Trauma, such as an injury during contact sports
• Cancer that has spread (metastasized) to the spleen
• A cyst, a noncancerous fluid-filled sac
  A large abscess, a pus-filled cavity usually caused by a bacterial infection
• Infiltrative diseases such as Gaucher disease, amyloidosis, or glycogen storage diseases splenic marginal zone lymphoma

Symptoms of Enlarge Spleen

An enlarged spleen may be caused by

• No symptoms in some cases
• Pain or fullness in the left upper abdomen that may spread to the left shoulder
• Feeling full without eating or after eating only a small amount from the enlarged spleen pressing on your stomach
• pressure or pain in the left upper part of your abdomen (near the stomach),
• feeling full without eating a large meal,
• or pain your left shoulder blade or shoulder area when taking a deep breath.
• Anemia
• Fatigue
• Frequent infections
• Easy bleeding

Diagnosis of Enlarged Spleen

History and Physical

The most common physical symptom associated with splenomegaly is vague abdominal discomfort. Patients may complain of pain in the left upper abdomen or referred pain in the left shoulder. Abdominal bloating, distended abdomen, anorexia, and/or early satiety may also occur. More commonly, patients will present with symptoms due to the underlying illness causing splenomegaly. Constitutional symptoms such as weakness, weight loss, and night sweats suggest malignant illness. Patients with splenomegaly due to acute infection may present with fever, rigors, generalized malaise, or focal infectious symptoms. Patients with underlying liver disease may present with symptoms related to cirrhosis or hepatitis. Symptoms of anemia (lightheadedness, dyspnea, or exertion), easy bruising, bleeding, or petechiae may indicate splenomegaly due to the underlying hemolytic process.

Physical examination of the spleen is performed with the patient in supine and right lateral decubitus position with neck, hips, and knees flexed. This positioning relaxes abdominal wall musculature and rotates the spleen more anteriorly. Light fingertip pressure is applied below the left costal margin during deep inspiration. The examiner may feel the rounded edge of the spleen pass underneath the fingertips at maximum inspiration. The exam is abnormal if the spleen is palpated more than 2 cm below the costal margin. In massive splenomegaly, the spleen may be palpated deep into the abdomen, crossing the midline of the abdomen and may even extend into the pelvis. Studies have shown that normal sized spleens may be palpable in approximately 3% of adults.

Patients may have an abnormally palpable spleen with or without exam findings of contributing underlying illness. Patients with splenomegaly due to acute infection may have exam findings consistent with infectious mononucleosis, endocarditis, or malaria. Exam findings of petechiae, abnormal mucosal bleeding, or pallor may accompany hematologic diseases. Jaundice, hepatomegaly, ascites, or spider angiomata may be present in patients with liver disease.  Patients with rheumatologic diseases may present with joint tenderness, swelling, rash, or an abnormal lung exam.

Evaluation

A combination of serum testing and imaging studies may definitively diagnose splenomegaly and the underlying cause. Derangement in the complete blood (cell) counts and morphology including WBC, RBC, and platelets will vary based on the underlying disease state. Abnormalities in liver function tests, lipase, rheumatologic panels, and disease-specific infectious testing aid in the diagnosis of causative disease.[rx] Hypersplenism may present with leukopenia, anemia, and thrombocytopenia.

Investigations

Investigations for splenomegaly should be targeted to the most likely underlying cause and include:

• Blood tests – FBC/blood film/U+E/LFTs/LDH/autoimmune screen/blood culturesHIV test
• CXR – looking for bihilar lymphadenopathy which may suggest an underlying lymphoproliferative process or infection. Malaria film if recent foreign travel to a malaria-endemic area Echo if infective endocarditis is suspected
• CT thorax abdop Elvis  – if underlying malignancy suspected. Bone marrow aspirate and trephine if an underlying hematological process is likely
• Lymph node biopsy – Imaging may be used to diagnose splenomegaly and elucidate its underlying cause. The spleen has a similar attenuation as the liver when measured on CT imaging. In addition to diagnosing splenomegaly (a splenic measurement of greater than 10 cm in craniocaudal length), abdominal CT may detect splenic abscess, mass lesions, vascular abnormalities, cysts, inflammatory changes, traumatic injury, intra-abdominal lymphadenopathy, or liver abnormalities.
• Sonography in trauma (FAST) exam – uses ultrasound to assess for the presence of fluid where it should not be in trauma evaluation. A FAST exam looks at four windows: pericardial window, Morrison’s pouch (right upper quadrant between liver and right kidney), left upper quadrant (between the spleen and left kidney), and the suprapubic region to look at the bladder and pelvis. The exam is considered positive with fluid in any of these spaces, and combination with hemodynamic instability is an indication for exploratory laparotomy. With positive fluid in the pericardial window, a pericardiocentesis is an appropriate followup.[rx]
• Computed tomography (CT) – are beneficial tools to visualize and characterize the spleen. Both modalities function to measure the spleen and identify physical abnormalities. While not necessary, the use of contrast can aid in tracing blood flow and help identify any leaks or pathologic fluid collection.[rx]
• Ultrasound – is a useful imaging modality in measuring the spleen and spares the patient radiation from CT imaging. Normal spleen size measured via ultrasound is less than 13 cm superior to the inferior axis, 6 cm to 7 cm in medial to lateral axis and 5 cm to 6 cm in anterior to the posterior plane.
• MRI, PET scans – liver-spleen colloid scanning, and splenectomy and splenic biopsy may be indicated in certain cases.

Treatment of Enlarge Spleen

Treatment of splenomegaly is targeted at treating the underlying disease and protecting the patient from complications of splenomegaly itself.  Patients with splenomegaly from any cause are at increased risk of splenic rupture, and increased attention must be made to protect the patient from abdominal trauma. Treatment ranges from abdominal injury avoidance in the young healthy patient with splenomegaly due to infectious mononucleosis, to splenectomy of a massively enlarged spleen in a patient with hairy cell leukemia. Likewise, the prognosis is largely dependent on the underlying disease state.[rx][rx]

• Splenic sequestration – is seen in sickle cell anemia is often managed with blood transfusions/exchange transfusions. Sometimes splenectomy is required for ITP. Low dose radiation therapy can also shrink the spleen size in patients with primary myelofibrosis.
• Patients who undergo splenectomy – are at increased risk of infections secondary to encapsulated organisms such as Haemophilus Influenzae, Streptococcus pneumonia, and Neisseria meningitides. Vaccinations against these organisms are highly recommended in patients who have undergone splenectomy. Careful attention must be paid to post-splenectomy patients presenting with febrile illnesses as they may require more aggressive, empiric antibiotic therapy.
• If the splenomegaly underlies hypersplenism – splenectomy is indicated and will correct the hypersplenism. However, the underlying cause of hypersplenism will most likely remain; consequently, a thorough diagnostic workup is still indicated, as, leukemia, lymphoma and other serious disorders can cause hypersplenism and splenomegaly. After splenectomy, however, patients have an increased risk for infectious diseases.
• Infective endocarditis suspected – TTE (transthoracic) +/- TOE (transoesophageal) for vegetations, at least 3 different sets of blood cultures from different sites at the different time should be sent and discuss with cardiology and microbiology for appropriate treatment

Patients undergoing splenectomy should be vaccinated against Haemophilus influenzae, Streptococcus pneumoniae, and Meningococcus. They should also receive annual influenza vaccinations. Long-term prophylactic antibiotics may be given in certain cases.

Differential Diagnosis

There are several potential causes of splenomegaly, and careful and thorough evaluation is often needed to find the underlying cause of splenomegaly.

These include:

• Cirrhosis
• Hepatitis
• Rheumatoid arthritis
• Felty syndrome
• Systemic lupus erythematosus
• Lymphoma
• Sickle cell anemia

Liver disease (cirrhosis, hepatitis) is one of the most common causes and history of liver disease, abnormal physical exam findings and elevated liver enzymes in addition to abnormal liver imaging can help diagnose liver diseases.

Hematologic malignancies and metastasis shall be especially considered in patients with constitutional symptoms and weight loss. Abnormal peripheral blood smear and biopsy can assist in diagnosing malignancies.

Autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) frequently are associates with splenomegaly. In RA, the presence of splenomegaly in addition to neutropenia is termed Felty syndrome.

Acute and chronic infections including viral, bacterial, fungal, and mycobacterial infections can all cause splenomegaly and shall be carefully ruled out.

Cytopenias and diseases causing splenic sequestration can be ruled out by complete blood counts, peripheral blood smear and hemoglobin electrophoresis.

Infiltrative disorders such as glycogen storage diseases are a rare cause of splenomegaly and shall be considered if other more common causes are ruled out in patients with other clinical features consistent with these glycogen storage diseases.

References

Splenomegaly is defined as enlargement of the spleen measured by weight or size. The spleen plays a significant role in hematopoiesis and immunosurveillance. The major functions of the spleen include clearance of senescent and abnormal erythrocytes and their remnants, opsonized platelets and white blood cells and removal of microorganisms and antigens. The spleen also serves as a secondary lymphoid organ and is the site for maturation and storage of T and B lymphocytes, playing an important role in the synthesis of immunoglobulin G (IgG) by mature B-lymphocytes upon interaction with the T-lymphocytes.  The spleen also synthesizes the immune system peptides properdin and tuftsin. Approximately one-third of circulating platelets are stored in the spleen. The normal position of the spleen is within the peritoneal cavity in the left upper quadrant adjacent to ribs 9 through 12. The normal-sized spleen abuts the stomach, colon, and left kidney.

The size and weight of spleen may vary and correlates with weight, height, and sex of an individual, with larger spleen size seen in men compared to women, and in heavier or taller individuals. A normally sized spleen measures up to 12 cm in craniocaudal length.  A length of 12 cm to 20 cm indicates splenomegaly, and a length greater than 20 cm is definitive of massive splenomegaly. The normal weight of the adult spleen is 70 g to 200 g; a spleen weight of 400 g to 500 g indicates splenomegaly and a spleen weight greater than 1000 g is definitive of massive splenomegaly. The normal-sized spleen is usually not palpable in adults. However, it may be palpable due to variations in body habitus and chest wall anatomy. Splenomegaly may be diagnosed clinically or radiographically using ultrasound, CT imaging, or MRI.  Splenomegaly may be a transient condition due to acute illness or may be due to serious underlying acute or chronic pathology.[rx][rx][rx]

Splenomegaly is an enlargement of the spleen.^[rx] The spleen usually lies in the left upper quadrant (LUQ) of the human abdomen. Splenomegaly is one of the four cardinal signs of hypersplenism which include: some reduction in the number of circulating blood cells affecting granulocytes, erythrocytes, or platelets in any combination; a compensatory proliferative response in the bone marrow; and the potential for correction of these abnormalities by splenectomy. Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a response to hyperfunction. It is therefore not surprising that splenomegaly is associated with any disease process that involves abnormal red blood cells being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by leukemias and lymphomas. Thus, the finding of an enlarged spleen, along with caput-medusae, is an important sign of portal hypertension.^[rx]

Types of Splenomegaly

Splenomegaly can be classified based on its pathophysiologic mechanism:

• Congestive – by pooled blood (e.g., portal hypertension)
• Infiltrative – by invasion by cells foreign to the splenic environment (e.g., metastases, myeloid neoplasms, lipid storage diseases)
• Immune – by an increase in immunologic activity and subsequent hyperplasia (e.g., endocarditis, sarcoidosis, rheumatoid arthritis)
• Neoplastic – when resident immune cells originate a neoplasm (e.g., lymphoma).

The standard system for classifying splenomegaly on radiography is:^[rx][rx]

• Normal (not splenomegaly) – the largest dimension is less than 11 cm
• Moderate splenomegaly – the largest dimension is between 11–20 cm
• Severe splenomegaly – the largest dimension is greater than 20 cm

Causes of Splenomegaly

There are several potential causes of splenomegaly.

• Liver disease (cirrhosis, hepatitis): Parenchymal liver disease causes increased vascular pressure leading to an increase in spleen size.
• Hematologic malignancies (lymphomas, leukemias, myeloproliferative disorders): Neoplastic cells cause infiltration of the spleen leading to splenomegaly.
• Venous thrombosis (portal or hepatic vein thrombosis): This leads to an increase in vascular pressure leading to splenomegaly.
• Splenic congestion (venous thrombosis, portal hypertension, congestive heart failure).
• Cytopenias (Immune thrombocytopenic purpura, autoimmune hemolytic anemia, immune-mediated neutropenia, Felty syndrome): Immune-mediated destruction of red blood cells, white blood cells or platelets lead to functional splenomegaly.
• Splenic sequestration (pediatric sickle cell disease, hemolytic anemias, thalassemias).
• Acute or chronic infection (bacterial endocarditis, infectious mononucleosis, HIV, malaria, tuberculosis, histiocytosis, abscess).
• Connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis, Adult-onset Still’s disease, and some familial autoinflammatory syndromes).[rx][rx]
• Infiltrative disorders (sarcoidosis, amyloidosis, glycogen storage diseases).
• Splenic sequestration (pediatric sickle cell, hemolytic anemias, thalassemias).
• Focal lesions (hemangiomas, abscess, cysts, metastasis).
• malaria
• Hodgkin’s disease
• leukemia
• heart failure
• cirrhosis
• tumors in the spleen or from other organs that have spread to the spleen
• viral, bacterial, or parasitic infections
• inflammatory diseases, such as lupus or rheumatoid arthritis
• sickle cell disease

The mechanism underlying splenic enlargement varies based on the etiology. In the case of acute infectious illness, the spleen performs increased work in clearing antigens and producing antibodies and increases the number of reticuloendothelial cells contained within the spleen. These increased immune functions may result in splenic hyperplasia. In the case of liver disease and congestion, underlying illness causes increased venous pressure causing congestive splenomegaly. Extramedullary hematopoiesis exhibited in myeloproliferative disorders can lead to splenic enlargement (infiltrative splenomegaly).[rx][rx]

The possible causes of moderate splenomegaly (spleen <1000 g) are many and include

The causes of massive splenomegaly (spleen >1000 g) are

• chronic myelogenous leukemia
• myelofibrosis
• malaria
• Inflammatory diseases such as sarcoidosis, lupus, and rheumatoid arthritis
• Trauma, such as an injury during contact sports
• Cancer that has spread (metastasized) to the spleen
• A cyst, a noncancerous fluid-filled sac
  A large abscess, a pus-filled cavity usually caused by a bacterial infection
• Infiltrative diseases such as Gaucher disease, amyloidosis, or glycogen storage diseases splenic marginal zone lymphoma

Symptoms of Splenomegaly

An enlarged spleen may be caused by

• No symptoms in some cases
• Pain or fullness in the left upper abdomen that may spread to the left shoulder
• Feeling full without eating or after eating only a small amount from the enlarged spleen pressing on your stomach
• pressure or pain in the left upper part of your abdomen (near the stomach),
• feeling full without eating a large meal,
• or pain your left shoulder blade or shoulder area when taking a deep breath.
• Anemia
• Fatigue
• Frequent infections
• Easy bleeding

Diagnosis of Splenomegaly

History and Physical

The most common physical symptom associated with splenomegaly is vague abdominal discomfort. Patients may complain of pain in the left upper abdomen or referred pain in the left shoulder. Abdominal bloating, distended abdomen, anorexia, and/or early satiety may also occur. More commonly, patients will present with symptoms due to the underlying illness causing splenomegaly. Constitutional symptoms such as weakness, weight loss, and night sweats suggest malignant illness. Patients with splenomegaly due to acute infection may present with fever, rigors, generalized malaise, or focal infectious symptoms. Patients with underlying liver disease may present with symptoms related to cirrhosis or hepatitis. Symptoms of anemia (lightheadedness, dyspnea, or exertion), easy bruising, bleeding, or petechiae may indicate splenomegaly due to the underlying hemolytic process.

Physical examination of the spleen is performed with the patient in supine and right lateral decubitus position with neck, hips, and knees flexed. This positioning relaxes abdominal wall musculature and rotates the spleen more anteriorly. Light fingertip pressure is applied below the left costal margin during deep inspiration. The examiner may feel the rounded edge of the spleen pass underneath the fingertips at maximum inspiration. The exam is abnormal if the spleen is palpated more than 2 cm below the costal margin. In massive splenomegaly, the spleen may be palpated deep into the abdomen, crossing the midline of the abdomen and may even extend into the pelvis. Studies have shown that normal sized spleens may be palpable in approximately 3% of adults.

Patients may have an abnormally palpable spleen with or without exam findings of contributing underlying illness. Patients with splenomegaly due to acute infection may have exam findings consistent with infectious mononucleosis, endocarditis, or malaria. Exam findings of petechiae, abnormal mucosal bleeding, or pallor may accompany hematologic diseases. Jaundice, hepatomegaly, ascites, or spider angiomata may be present in patients with liver disease.  Patients with rheumatologic diseases may present with joint tenderness, swelling, rash, or an abnormal lung exam.

Evaluation

A combination of serum testing and imaging studies may definitively diagnose splenomegaly and the underlying cause. Derangement in the complete blood (cell) counts and morphology including WBC, RBC, and platelets will vary based on the underlying disease state. Abnormalities in liver function tests, lipase, rheumatologic panels, and disease-specific infectious testing aid in the diagnosis of causative disease.[rx] Hypersplenism may present with leukopenia, anemia, and thrombocytopenia.

Investigations

Investigations for splenomegaly should be targeted to the most likely underlying cause and include:

• Blood tests – FBC/blood film/U+E/LFTs/LDH/autoimmune screen/blood culturesHIV test
• CXR – looking for bihilar lymphadenopathy which may suggest an underlying lymphoproliferative process or infection. Malaria film if recent foreign travel to a malaria-endemic area Echo if infective endocarditis is suspected
• CT thorax abdop Elvis  – if underlying malignancy suspected. Bone marrow aspirate and trephine if an underlying hematological process is likely
• Lymph node biopsy – Imaging may be used to diagnose splenomegaly and elucidate its underlying cause. The spleen has a similar attenuation as the liver when measured on CT imaging. In addition to diagnosing splenomegaly (a splenic measurement of greater than 10 cm in craniocaudal length), abdominal CT may detect splenic abscess, mass lesions, vascular abnormalities, cysts, inflammatory changes, traumatic injury, intra-abdominal lymphadenopathy, or liver abnormalities.
• Sonography in trauma (FAST) exam – uses ultrasound to assess for the presence of fluid where it should not be in trauma evaluation. A FAST exam looks at four windows: pericardial window, Morrison’s pouch (right upper quadrant between liver and right kidney), left upper quadrant (between the spleen and left kidney), and the suprapubic region to look at the bladder and pelvis. The exam is considered positive with fluid in any of these spaces, and combination with hemodynamic instability is an indication for exploratory laparotomy. With positive fluid in the pericardial window, a pericardiocentesis is an appropriate followup.[rx]
• Computed tomography (CT) – are beneficial tools to visualize and characterize the spleen. Both modalities function to measure the spleen and identify physical abnormalities. While not necessary, the use of contrast can aid in tracing blood flow and help identify any leaks or pathologic fluid collection.[rx]
• Ultrasound – is a useful imaging modality in measuring the spleen and spares the patient radiation from CT imaging. Normal spleen size measured via ultrasound is less than 13 cm superior to the inferior axis, 6 cm to 7 cm in medial to lateral axis and 5 cm to 6 cm in anterior to the posterior plane.
• MRI, PET scans – liver-spleen colloid scanning, and splenectomy and splenic biopsy may be indicated in certain cases.

Treatment of Splenomegaly

Treatment of splenomegaly is targeted at treating the underlying disease and protecting the patient from complications of splenomegaly itself.  Patients with splenomegaly from any cause are at increased risk of splenic rupture, and increased attention must be made to protect the patient from abdominal trauma. Treatment ranges from abdominal injury avoidance in the young healthy patient with splenomegaly due to infectious mononucleosis, to splenectomy of a massively enlarged spleen in a patient with hairy cell leukemia. Likewise, the prognosis is largely dependent on the underlying disease state.[rx][rx]

• Splenic sequestration – is seen in sickle cell anemia is often managed with blood transfusions/exchange transfusions. Sometimes splenectomy is required for ITP. Low dose radiation therapy can also shrink the spleen size in patients with primary myelofibrosis.
• Patients who undergo splenectomy – are at increased risk of infections secondary to encapsulated organisms such as Haemophilus Influenzae, Streptococcus pneumonia, and Neisseria meningitides. Vaccinations against these organisms are highly recommended in patients who have undergone splenectomy. Careful attention must be paid to post-splenectomy patients presenting with febrile illnesses as they may require more aggressive, empiric antibiotic therapy.
• If the splenomegaly underlies hypersplenism – splenectomy is indicated and will correct the hypersplenism. However, the underlying cause of hypersplenism will most likely remain; consequently, a thorough diagnostic workup is still indicated, as, leukemia, lymphoma and other serious disorders can cause hypersplenism and splenomegaly. After splenectomy, however, patients have an increased risk for infectious diseases.
• Infective endocarditis suspected – TTE (transthoracic) +/- TOE (transoesophageal) for vegetations, at least 3 different sets of blood cultures from different sites at the different time should be sent and discuss with cardiology and microbiology for appropriate treatment

Patients undergoing splenectomy should be vaccinated against Haemophilus influenzae, Streptococcus pneumoniae, and Meningococcus. They should also receive annual influenza vaccinations. Long-term prophylactic antibiotics may be given in certain cases.

Differential Diagnosis

There are several potential causes of splenomegaly, and careful and thorough evaluation is often needed to find the underlying cause of splenomegaly.

These include:

• Cirrhosis
• Hepatitis
• Rheumatoid arthritis
• Felty syndrome
• Systemic lupus erythematosus
• Lymphoma
• Sickle cell anemia

Liver disease (cirrhosis, hepatitis) is one of the most common causes and history of liver disease, abnormal physical exam findings and elevated liver enzymes in addition to abnormal liver imaging can help diagnose liver diseases.

Hematologic malignancies and metastasis shall be especially considered in patients with constitutional symptoms and weight loss. Abnormal peripheral blood smear and biopsy can assist in diagnosing malignancies.

Autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) frequently are associates with splenomegaly. In RA, the presence of splenomegaly in addition to neutropenia is termed Felty syndrome.

Acute and chronic infections including viral, bacterial, fungal, and mycobacterial infections can all cause splenomegaly and shall be carefully ruled out.

Cytopenias and diseases causing splenic sequestration can be ruled out by complete blood counts, peripheral blood smear and hemoglobin electrophoresis.

Infiltrative disorders such as glycogen storage diseases are a rare cause of splenomegaly and shall be considered if other more common causes are ruled out in patients with other clinical features consistent with these glycogen storage diseases.

References

Homeopathic medicines cannot cure hemiplegia. However, the medicines can be administered to improve the state of paralysis, improve blood circulation, help control loss of power, improve the power of muscles to come extent and improve the overall health of the patient.

Some common medicines for hemiplegia and such states of paralysis are:

• Plumbum Metallicum – This medicine is sourced by processing and potentizing the metal lead. It helps the neuro-muscular system of the body. It is administered with the intention to improve some muscle power. Plumbum met, as it is called, may be indicated all kinds of paralysis such as hemiplegia, paraplegia, and quadriplegia. As said earlier, it cannot cure paralysis as such.
• Causticum – Similar to the above medicine, Causticum is also a friend to all paralysis patients. It is aimed at improving some muscle power and not cure it.
• Nux vomica – This herbal medicine helps in the early stages of hemiplegia and not after some months or years.
• Lathyrus sativus – This is another example of a toxin transformed into medicine. It is safe, There are some spasticity and stiffness in some muscles, in the cases of hemiplegia, where Lathyrus may be called for.
• Gelsemium – This plant remedy is useful for early cases of paralysis including hemiplegia. It is supposed to improve muscle strength in the cases of paralysis.

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Prevention

Reducing the number of controllable risk factors is the best way to prevent a stroke.  This can include:

• Stopping smoking
• Losing weight
• Eating a balanced diet low in sodium and saturated and trans fat
• Moderating alcohol intake (no more than 2 small drinks per day)
• Exercising regularly in order to stay physically fit
• Maintaining good control of existing medical conditions such as diabetes, high blood pressure and high cholesterol.

Referances