Other possible syndromes include thyroid storm and withdrawal from benzodiazepines or ethanol. Autonomic instability, including fever, diaphoresis, tachycardia, hyper- or hypotension, mydriasis. History of use of serotonin-based antidepressants or other drugs associated with serotonin release. Supportive Measures-Basic supportive measures such as intravenous fluid administration and supplemental oxygen should be initiated as indicated by the clinical situation. When hyperthermia is present, the patient should be undressed completely and sprayed with a cool mist or draped with a wet sheet. Specific Treatment-Potential drugs precipitating the serotonin syndrome should be discontinued. They are anticonvulsants, are not associated with serotonin release, and are anxiolytic and sedating. Dantrolene uncouples excitation-contract in skeletal muscles and has been used in malignant hyperthermia, neuroleptic malignant syndrome, and serotonin syndrome. There are case reports of benefit from dantrolene in serotonin syndrome but no controlled trials. However, chlorpromazine may be contraindicated in neuroleptic malignant syndrome because of its antidopaminergic properties. On the other hand, bromocriptine, a central dopaminergic agonist thought to be useful in neuroleptic malignant syndrome, may cause the serotonin syndrome and therefore is contraindicated. One approach is to treat with benzodiazepines as necessary while carefully supporting the patient and considering the need for dantrolene and cyproheptadine. This produces vasodilation and negative inotropic, dromotropic, and chronotropic activity. The most commonly used calcium channel blockers are verapamil, diltiazem, and nifedipine, and each has slightly different effects. Clinical Features Although toxicity is seen most frequently with oral ingestion, significant -blocker toxicity also can be seen in patients being treating with -blocker eyedrops for conditions such as glaucoma. Patients with significant -blockade toxicity present with bradycardia, conduction blocks, hypotension, decreased cardiac output, and cardiogenic shock; depressed mental status also may be seen. Bradycardia can be severe and appears to be more common with ingestions of propranolol than with other drugs. Overdose with atenolol, nadolol, carvedilol, and metoprolol tend to present with hypotension and a heart rate that may be within normal limits. Pindolol and practolol overdoses may present with tachycardia owing to their partial agonist activity. First-degree atrioventricular block is common with propranolol overdoses, and junctional rhythms, bundle branch block, complete atrioventricular block, and asystole all have been observed with -blocker ingestions. Depressed mental status is also seen frequently and is more common in patients with significant hypotension. Significant calcium channel blocker overdose commonly presents with bradycardia, hypotension, and significant heart block (including third-degree heart block), which can be lifethreatening. These patients also may be somewhat drowsy, although markedly altered mental status is rare. Differential Diagnosis -Blocker overdoses present with bradycardia and hypotension; these findings also can occur with barbiturate intoxication and in cases of ingestion of some antiarrhythmics such as mexiletine. General Considerations Acute overdose of -blockers and calcium channel blockers can be potentially life-threatening and poses significant treatment challenges for the intensivist. Clinical manifestations of -blocker overdose are due to the effects of systemic -adrenergic blockade. Decontamination-In both -blocker and calcium channel blocker overdoses, patients who present soon after ingestion of a significant amount of the drug should be considered for gastric lavage.
Pathology of pemphigus vulgaris is characterized by the in vivo deposition of an autoantibody on the keratinocyte cell surface. This antibody, which is also present in the circulation, is typically directed against a 130-kDa protein (desmoglein 3). Histology reveals the presence of a suprabasilar intraepidermal split with acantholysis. There are deposits of IgG and C3 on the corticokeratinocyte cell surface in the mid and lower or entire epidermis of perilesional skin or mucosa. In some reports titers of IgG4 antikeratinocyte antibodies correlated with disease activity. Current management/treatment the treatment of pemphigus vulgaris, especially in its severe form, is challenging. Introduction of corticosteroids reduced the mortality rate from 70 to 100% to a mean of 30%. However, long-term administration of high doses of corticosteroids can be associated with severe adverse effects. They are often used in combination with other immunosuppressant agents such as azathioprine, methotrexate, and cyclophosphamide. In addition, some newer experimental technologies involve cholinergic receptor agonists, desmoglein 3 peptides and a p38 mitogen activated protein kinase inhibitor. All reported patients have received high-dose systemic corticosteroids and immunosuppressive agents which either produced life-threatening adverse effects or failed to control the disease. The study, though not powered to answer the question of clinical benefit, underlines the potential side effects of immunosuppressive therapy. The reported volume processed was as low as 400 mL and as high as 4,000 mL and the reported frequency of treatments varied widely as well. Though, more recent reports noted that one plasma volume exchanges are preferable in patients who are resistant to conventional therapy. In one report 100% clinical response with decreased autoantibody titer was reported. The disease was controlled in most patients, but only two patients were able to discontinue all oral systemic agents. The rational approach should include monitoring of autoantibody titers and clinical symptoms. The lack of clinical response after a trial period with concomitant adequate immunosuppression should be sufficient to discontinue treatment. Clinical consequences are largely neurological including retinitis pigmentosa, peripheral neuropathy, cerebellar ataxia, sensorineural deafness and anosmia. Other manifestations include skeletal abnormalities, cardiac arrhythmia and ichthiosis. The clinical progression is typically slow and gradual with onset of signs and symptoms during the 2nd or 3rd decades of life due to the gradual accumulation of phytanic acid from dietary sources. Progression of symptoms can lead to retinitis pigmentosa, and possibly loss of sight. Patients with cardiac manifestation may experience arrhythmias which could be fatal or prompt cardiac transplantion. The specific biochemical basis for the accumulation of phytanic acid in these patients is related to an enzyme defect in phytanoyl-CoA hydrolase. Diet alone can benefit many patients and lead to reversal of neuropathy, weakness and icthiosis. A number of small case series and isolated reports have described clinical improvements in patient signs and symptoms with plasma exchange in conjunction with dietary control. Unfortunately, as is also reported with dietary treatment alone, the visual, olfactory, and hearing deficits do not respond. Patients may experience severe exacerbations of disease during episodes of illness or weight loss, such as during the initiation of dietary management.
Fluid losses may be so severe that hypotension results and ultimately may lead to cardiovascular collapse unless recognized and treated expeditiously. Vomiting usually accompanies small bowel obstruction and becomes progressively more feculent as the illness progresses. Respiration is adversely affected by abdominal distention and impaired diaphragmatic excursion. Closed-loop obstruction is a feared consequence of complete mechanical obstruction. When it occurs, no outlet for the accumulated intraluminal contents exists, and perforation of the bowel may occur. Strangulation rarely results from progressive distention, although venous outflow becomes significantly impaired as the bowel and mesentery continue to distend. Free perforation occurs as a consequence of gangrene, releasing the highly toxic stagnant intraluminal mixture of bacterial products, live bacteria, necrotic tissue, and blood. There are no specific historical, physical, or laboratory findings that exclude the possibility of strangulation in complete small bowel obstruction, which occurs in approximately one-third of patients. The early appearance of shock, gross hematemesis, and profound leukocytosis suggests the presence of a strangulated obstruction. Symptoms and Signs-Obstruction of the proximal small bowel usually presents with vomiting. The extent of associated abdominal pain is variable and usually is described as intermittent or colicky with a crescendodecrescendo pattern. When the obstruction is located in the middle or high small bowel (jejunum and proximal ileum), the pain may be more constant. As loss of fluid and electrolytes continues, dehydration occurs, manifested as tachycardia and postural hypotension. It is more pronounced with distal obstruction and when more proximal lesions have been allowed to progress without decompression. Dilated loops of small bowel may be visible beneath the abdominal wall in thin patients. Characteristic peristaltic rushes, gurgles, and high-pitched tinkles may be audible and occur in synchrony with cramping pain. Variable manifestations of obstruction depend on the level of blockage of the small bowel. With progression, there is hemoconcentration, leukocytosis, and electrolyte abnormalities whose extent and nature depend in part on the level of obstruction present. Imaging Studies-On plain abdominal films, a ladderlike pattern of dilated small bowel loops and air-fluid levels will be noted, particularly in distal obstruction. If a gallstone precipitated the event, it may be noted on the film, or air may be seen in the biliary tree. When strangulation and necrosis occur, loss of mucosal regularity, gas within the bowel wall, and "thumbprinting" of the bowel wall occur. Free air on an upright chest x-ray is highly suggestive of intestinal perforation. Contrast studies are usually not required and should not be performed because of the risk of barium peritonitis if a perforation is present. However, in patients with high-grade partial obstructions who are poor surgical risks, administration of a dilute barium mixture through the nasogastric tube can be used to determine whether a residual lumen is still present for the passage of gas and liquid contents. Differential Diagnosis Ileus is a prominent feature of the differential diagnosis. It can be caused by a number of intraabdominal and retroperitoneal processes, including intestinal ischemia, ureteral colic, pelvic fractures, and back injuries. If paralytic ileus is present, the pain is usually not as severe and tends to be more constant. Obstipation and abdominal distention characterize obstruction of the large intestine. The diagnosis is usually made on the basis of x-ray findings that show colonic dilation proximal to the point of obstruction. Small bowel obstruction can be confused with acute gastroenteritis, acute appendicitis, and acute pancreatitis. Strangulating obstructions may be mimicked by acute pancreatitis, ischemic enteritis, or mesenteric vascular occlusion owing to venous thrombosis.
Examples include amphetamine and its derivatives, overthe-counter products for appetite control, cold remedies, and stimulants (eg, phenylpropanolamine, caffeine, ephedrine, and pseudoephedrine). Overuse of sympathomimetics causes toxicity by inducing excessive release of neurotransmitters, including epinephrine and norepinephrine, and the subsequent - and -adrenergic effects they produce. The clinical effects that result from any specific sympathomimetic drug depend on the relative - or -adrenergic actions of that drug (eg, phenylpropanolamine is an -selective drug that causes hypertension, diaphoresis, and mydriasis). Duration of toxicity is usually limited; however, patients may demonstrate prolonged toxicity if they ingest bags containing the drug for illicit transport or if they use "Ice," a long-acting, smokable form of methamphetamine. Because the half-life of naloxone is substantially shorter than that of most narcotic agents, repeat dosing may be required to prevent recurrence of respiratory and mental status depression. Continuous administration of naloxone intravenously may be required in some cases to prevent relapse of respiratory depression. Rhabdomyolysis may occur, particularly in patients who have been obtunded for a significant amount of time; if not treated, patients may develop renal failure from the myoglobinuria seen in this condition. Withdrawal Withdrawal from narcotics produces autonomic disturbances, hyperexcitability, and personality changes characterized by drug-seeking behavior. Within the first 8 hours of withdrawal, lacrimation, rhinorrhea, diaphoresis, and sneezing are common. Both illicit drug users and those who use excessive amounts of over-the-counter medications (eg, diet aids, stimulants, and cold medications) may present with sympathomimetic poisoning. Sympathomimetics may cause a psychotic state indistinguishable from that seen in schizophrenia; although almost always temporary, this psychosis may take weeks to months to resolve. Less common but more severe effects include coma, strokes (ischemic and hemorrhagic), hypertensive encephalopathy, and focal neurologic deficits. Sinus bradycardia or atrioventricular block occurs mainly after ingestion of drugs with primarily -agonist properties. Other findings include rhabdomyolysis with or without renal failure, diarrhea, intestinal cramping, and hyperthermia. Toxicology screening may be positive for sympathomimetic drugs, but it is by no means comprehensive of the wide array of available agents; therefore, a negative screen does not exclude sympathomimetic toxicity. Leukocytosis is common as a result of demargination caused by catecholamine stimulation. Although nifedipine is a potent antihypertensive agent, it is not easily titrated, and cases of prolonged hypotension from its use have been reported. Supraventricular tachycardia is usually benign; however, when the patient suffers compromise from the rapid ventricular response, verapamil or adenosine may be used to control the rhythm. Esmolol may be used to treat both supraventricular tachycardia and ventricular dysrhythmias. Esmolol and other -adrenergic blockers may worsen hypertension because of unopposed -adrenergic activity. Status epilepticus may develop and may require treatment with phenobarbital and phenytoin. If these medications are ineffective, paralysis may be required to prevent rhabdomyolysis, acidosis, and hyperthermia. Continuous electroencephalographic monitoring is required in these patients because they may continue to have electrical seizure activity despite chemical paralysis. Psychosis-Benzodiazepines may be used to treat psychosis associated with sympathomimetic overdoses. Although neuroleptics have been used in the past, they can lower the seizure threshold and alter thermoregulation; their use probably should be avoided in this situation. Myocardial Ischemia-Although actual myocardial infarction is rare, patients with angina pectoris should be managed with aspirin, nitrates, and heart rate control. All clothing should be removed and patients sprayed with a mist of water or covered with damp sheets to increase evaporation, and a fan is helpful. Those with excessive agitation or seizures who do not respond to benzodiazepines may need paralysis to control heat production. A history of thyroid disease is suggestive of the diagnosis, as is the presence of goiter or physical findings suggestive of hyperthyroidism. Drug withdrawal (eg, ethanol and benzodiazepines) also presents with agitation and cardiovascular abnormalities. The agitation and paranoia seen in these patients may mimic psychiatric disorders such as schizophrenia. General Measures-After initial assessment and stabilization, treatment should be individualized to the drug involved and the toxic clinical effects manifest.
In pregnancy, progesterone mediates ureteral relaxation, predisposing to urinary stasis. In addition, compression of the ureters by the gravid uterus and engorged pelvic vessels is implicated. Obstetricians aggressively treat even asymptomatic lower tract infections because, untreated, 25% of such patients will progress to pyelonephritis. Pregnant women with pyelonephritis usually are treated as inpatients because of the greater incidence of severe complications of this disease in pregnancy. Treatment the mainstay of treatment is intravenous antibiotics, with an antimicrobial agent chosen empirically to cover the majority of community-acquired urinary pathogens. Since nausea and vomiting and anorexia frequently accompany pyelonephritis, volume depletion and dehydration are common and should be corrected promptly with intravenous crystalloid. The fever and dehydration of pyelonephritis frequently lead to premature uterine contractions. In addition, high maternal fevers have been shown to be associated with fetal neurologic harm. Because of the high risk of pulmonary damage in these patients, fluid overload should be avoided, and tocolytic drugs should be reserved for patients who demonstrate clear cervical changes. Even with adequate treatment, the patient with pyelonephritis may demonstrate a hectic fever course, although uncomplicated patients become afebrile after 48 hours. One group found that essentially all patients with pyelonephritis demonstrated evidence of hemolysis, sometimes leading to anemia and associated with bacterial endotoxins. Finally, the number of uterine contractions increases after the initiation of antibiotic therapy in some patients; this effect also has been attributed to the release of bacterial endotoxins. Treatment for endotoxin-mediated complications is symptomatic and supportive while antibiotics are continued. The possibility of endotoxin-mediated complications mandates close observation of pregnant patients with pyelonephritis even after antibiotics have been begun. This routinely should include continuous fetal heart rate monitoring in all pregnancies beyond 22 weeks of gestation. Even prior to this gestational age, maternal hypotension and hypoxemia should be detected and corrected before fetal injury results. These antibiotics can be administered orally on an outpatient basis after the patient becomes afebrile. After an episode of pyelonephritis, the pregnant patient is at increased risk for a recurrence. Often these patients are given antibiotic prophylaxis for the duration of the pregnancy and for 6 weeks postpartum. Symptoms and Signs-The typical patient presents with flank pain and fever of recent origin, often with rigors or chills. There may be a history of lower urinary tract infection, and many patients complain of concurrent lower tract symptoms such as dysuria and frequency. On physical examination, flank tenderness is usually present, more frequently on the right. Tachycardia of both mother and fetus may be present owing to fever and volume depletion. The presence of hypotension, tachypnea, extremely high fever, or marked tachycardia is ominous. Laboratory Findings-The urine nearly always contains white blood cells and bacteria, and red blood cells and casts are also seen frequently. The urine should be sent for culture to confirm the diagnosis and to check for antibiotic resistance. Differential Diagnosis In any febrile pregnant patient it is critical to exclude the diagnosis of intraamniotic infection. If any doubt exists, consideration should be given to performing amniocentesis to exclude this possibility.
Antihypertensive treatment usually is begun on an outpatient basis after documentation of persistent hypertension and evaluation for potentially reversible causes. A subset of patients present with or develop severe lifethreatening hypertension or have other coexisting medical problems requiring urgent control of blood pressure; these patients are defined as having a hypertensive crisis (sometimes called a hypertensive emergency). For example, patients with acute myocardial infarction or unstable angina benefit greatly from reduction of elevated blood pressure and lowering of left ventricular afterload. When congestive heart failure owing to left ventricular dysfunction or aortic or mitral regurgitation is associated with severe hypertension, rapid lowering of blood pressure will accelerate treatment of the hemodynamic dysfunction. Patients with acute aortic dissection and elevated blood pressure have greatly increased stress on the aorta, and urgent control of blood pressure is mandatory. Dilation of cerebral blood vessels results in hypertensive encephalopathy, and damage to the blood vessel wall can increase permeability, resulting in edema or bleeding. Malignant hypertension is defined by some as severe hypertension associated with specific end-organ damage, namely encephalopathy, nephropathy, or eye findings, including retinal hemorrhages, exudates, or papilledema. Treatment of malignant hypertension is important because rapid and effective lowering of blood pressure is essential for reversal of complications. Any of the causes of hypertension can be associated with hypertensive crisis, including essential, renovascular, or endocrine-mediated (eg, pheochromocytoma) forms of hypertension. The goal is to prevent permanent vascular and neurologic damage and to avoid worsening the heart failure or causing uncontrollable hypotension. Blood pressure should be controlled aggressively in these patients, and therapy should be instituted even while etiologic investigation is still under way. Of particular concern, patients with strokes or other types of neurologic dysfunction may sustain further neurologic damage if blood pressure is lowered too abruptly or excessively. Therefore, the initial goal of antihypertensive therapy within the first 6 hours is to lower the blood pressure by 25% of the starting blood pressure value or to no less than 150/110 mm Hg. Nitroprusside-Intravenous nitroprusside, which acts as a peripheral arteriodilator, is the drug of choice in hypertensive crises because it can be titrated rapidly and safely. Excessive hypotension can be avoided by careful blood pressure monitoring, usually with an arterial catheter, but a noninvasive automated cuff manometer is usually satisfactory. If hypotension occurs with nitroprusside therapy, discontinuation of the drug results in rapid restoration of blood pressure. However, over the first 24 hours, when control of blood pressure is essential, this is not a major concern. It should be avoided in patients with bronchospasm, severe heart failure, heart block, or bradycardia. Hydralazine is a peripheral vasodilator that can be given orally or intravenously. Reflex tachycardia is common, and -adrenergic blockers are almost always given simultaneously. The degree of lowering of blood pressure with intravenous nitroglycerin varies from patient to patient, and there is some risk of lowering cardiac output excessively with this drug. On the other hand, nitroglycerin has the advantage of being a coronary artery vasodilator and therefore is useful in patients with hypertension and myocardial ischemia. Symptoms and Signs-Patients with severely elevated blood pressure are frequently asymptomatic, but most will present with headache, confusion, stupor, seizure, or coma depending on the severity of the hypertension and the degree of end-organ involvement. Chest pain may be due to angina pectoris, unstable angina, or myocardial infarction associated with hypertension, but chest pain also should raise the possibility of aortic dissection. In malignant hypertension, papilledema, retinal hemorrhages, or exudates are present by definition and may be accompanied by encephalopathy. Acute oliguric renal failure as well as signs and symptoms of congestive heart failure may be seen.
Preoperative use of aspirin or other antiplatelet drugs may increase postoperative bleeding; if bleeding is severe and the bleeding time is prolonged, desmopressin or platelet transfusions may be required for control of bleeding. Surgery on the prostate gland or uterus may be associated with localized hyperfibrinolysis with excessive bleeding. Antifibrinolytic therapy with aminocaproic acid can be considered for control of bleeding (5-g loading dose followed by 1 g/h intravenously or orally until bleeding has stopped), although there is some risk of thrombi developing in the ureters (following prostate surgery) that are resistant to lysis. Acute renal failure owing to hypotension, massive blood loss, or medications can result in platelet dysfunction, which is exacerbated by anemia. Posttransfusion purpura with thrombocytopenia may occur in previously sensitized individuals. The use of intraoperative bovine thrombin as a hemostatic agent may precipitate the development of antibodies to thrombin and factor V. Hetastarch, a plasma volume expander, may cause persistent coagulation abnormalities, particularly in elderly patients, those with preexisting hemostatic defects, or with prolonged use. If bleeding is severe, plasmapheresis to remove these large molecules may be required to control bleeding. Medical treatment of hemostatic defects will depend on the specific abnormalities identified. If history and screening laboratory tests are unrevealing, consideration should be given to reexploration of the surgical site to identify adequacy of surgical hemostasis. Perioperative management of patients with inherited bleeding disorders requires preoperative collaboration among the surgeon, anesthesiologist, hematologist, and blood bank to ensure that optimal hemostasis is achieved during and after surgery. The details of therapy will depend on the nature of the specific disorder, the type of surgical procedure, and whether any additional medical complications are present. Severe coagulation disturbances associated with trauma may result in adrenal hemorrhage, which can further exacerbate hypotension. Pelvic ring fractures are associated with massive blood loss, often hidden owing to tracking of bleeding up into the retroperitoneal space. Control of bleeding in such circumstances may be difficult, even with aggressive blood product support-with fresh-frozen plasma, platelets, red blood cells, and cryoprecipitate. Perhaps as a consequence, these facilities are often associated with some of the most stressful psychiatric conditions within the hospital. Some regression generally occurs, however, as most patients experience stressors such as fear of death, enforced dependency, and potential permanent loss of function. They may try to cope with stress by suppressing their feelings, using humor to laugh at stressful aspects of their situation, or trying to anticipate a return to good health. If these techniques fail, the individual may turn to more primitive mechanisms such as projection, passive-aggressive maneuvers, acting-out behavior, and gross denial of illness. All this takes place during a time when the patient must deal with serious and usually multiple medical problems. It was believed to be due to the stress an ill individual felt in a foreboding environment with little privacy, lack of sleep, and sensory overload. Stress may play some role in producing delirium, but it is typically only a contributing one. The critical care physician should not automatically attribute delirium to stress. This aggressive approach is justified given the serious impact of delirium on morbidity and mortality in hospitalized patients. Studies have shown that patients suffering an episode of delirium have an increased risk of death, a longer hospital stay, and a greater need for subsequent nursing home placement. Memory impairment, when present, is generally global for both recent and remote events. The presence of delirium signifies primarily organic brain dysfunction and is not a manifestation of psychological distress alone. The signs and symptoms listed in the preceding paragraph are useful in making a clear-cut diagnosis. Indeed, one of the keys to diagnosis in these patients is repeated observations over time.
The main functions of crotalid venom are immobilization, death, and digestion of prey. Other components include metalloproteins, glycoproteins, lipids, and biogenic amines. Crotalid venom causes local tissue injury, coagulopathy, and systemic manifestations. The local injury is due to a combination of direct toxic damage to tissue as well as to ischemic damage owing to elevated compartment pressure resulting from local tissue edema. The coagulopathy is caused by procoagulant esterases that act on fibrinogen and split off fibrinopeptides. This results in depletion of fibrinogen and elevation of the prothrombin and partial thromboplastin times. Bradykinin is released by the action of arginine ester hydroxylase on plasma kininogen and may cause vasodilation and pooling of blood in the pulmonary and splanchnic beds, resulting in decreased venous return, hypotension, and shock. Myocardial ischemia and depression of contractility also have been associated with pit viper venom. Differential Diagnosis Identification of the type of snake is necessary to secure the appropriate antivenin. Remember that elapid bites may not result in local signs or symptoms despite envenomation. The primary survey and resuscitation should follow standard protocols available from the American College of Surgeons Advanced Trauma Life Support Course. The airway should be secured promptly in patients with envenomation to the head or neck. Antivenin-In the patient with major systemic signs and symptoms owing to severe envenomation, antivenin should be administered as quickly as possible. Antivenin is recommended for moderate to severe envenomation and for any envenomation with symptoms of progression-particularly worsening local injury, progressive coagulopathy, and hemolysis. A skin test is performed with the antivenin prior to administration in an attempt to predict the likelihood of an allergic reaction. Erythema and a wheal reaction within 30 minutes is a positive reaction indicating the need for treatment. The use of antivenin should be considered early because it may have to be obtained from a distance. Patients may require additional doses of antivenin if their symptoms progress after the initial administration. Mild reactions can be treated with intravenous diphenhydramine and epinephrine; severe reactions require increased doses. In cases of severe envenomation, further antivenin therapy should be strongly considered after treatment of a reaction. In less severe cases, antivenin should be withheld if possible after a reaction because there have been cases of death owing to anaphylaxis. Antivenin information can be obtained from local poison control centers or from a national service by calling 1-800-222-1222. Exotic envenomations may occur occasionally in the United States from foreign snakes or lizards kept in zoos or private collections. The principles of management are the same: supportive care and administration of appropriate antivenin. Most exotic antivenins are available at the institutions that maintain the snakes. The availability of these antivenins also can be determined through the Antivenin Index. Local Treatment-Local therapy consists of elevation and immobilization of the affected area until swelling recedes. If muscle compartments become firm, or if pain increases, the compartment pressure should be measured. Current Controversies and Unresolved Issues Immediate excision of the bite down to fascia and including damaged fascia and muscle has been advocated to reduce the incidence of local necrosis and to reduce systemic symptoms.
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