Shock metabolic acidosis with

Poisoning with iron-containing drugs produces vomiting, gross gastrointestinal bleeding, shock, metabolic acidosis, and coma and can be treated with supportive care and deferoxamine. 

Signs and symptoms Acute iron intoxication is most common in children and usually occure as a result of accidental ingestion of iron supplementation tablets. Depending on the dose, necrotizing gastroenteritis, shock, metabolic acidosis, coma, and death may result. Chronic toxicity occurs most often in individuals who must receive frequent transfusions (eg, patients with sickle cell anemia) and in those with hemochromatosis, an inherited abnormality of iron absorption. 

The authors reported that the clinical manifestations of coma, status epilepticus, cardiogenic shock, metabolic acidosis, and pulmonary edema were compatible with previously reported fatal cases of acute diphenhydramine poisoning. 

Respiratory and metabolic acidosis can develop in patients with cardiorespiratory arrest, with chronic lung disease and shock, and with metabolic acidosis and respiratory failure. 

Renal disease or renal dysfunction (eg, as suggested by serum creatinine levels greater than or equal to 1.5 mg/dL [males], greater than or equal to 1.4 mg/dL [females], or abnormal Ccr) that may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction (Ml), and septicemia CHF requiring pharmacologic treatment hypersensitivity to metformin acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Treat diabetic ketoacidosis with insulin. 

Shock is a complex acute cardiovascular syndrome that results in a critical reduction in perfusion of vital tissues and a wide range of systemic effects. Shock is usually associated with hypotension, an altered mental state, oliguria, and metabolic acidosis. If untreated, shock usually progresses to a refractory deteriorating state and death. The three major mechanisms responsible for shock are hypovolemia, cardiac insufficiency, and altered vascular resistance. Volume replacement and treatment of the underlying disease are the mainstays of the treatment of shock. Although sympathomimetic drugs have been used in the treatment of virtually all forms of shock, their efficacy is unclear. 

Normally, the sum of the cations exceeds the sum of the anions by no more than 12-16 mEq/L (or 8-12 mEq/L if the formula used for estimating the anion gap omits the potassium level). A larger-than expected anion gap is caused by the presence of unmeasured anions (lactate, etc) accompanying metabolic acidosis. This may occur with numerous conditions, such as diabetic ketoacidosis, renal failure, or shock-induced lactic acidosis. Drugs that may induce an elevated anion gap metabolic acidosis (Table 58-1) include aspirin, metformin, methanol, ethylene glycol, isoniazid, and iron. 

DKA is a positive anion gap metabolic acidosis associated with the accumulation of P-hydroxy-butyrate and acetoacetate. Lactic acidosis secondary to cardiac or renal failure, hypoxia, poor tissue perfusion, shock, or sepsis may also contribute to the anion gap in DKA. A normal anion gap (AG) is 12 2 mEq/L.The anion gap (AG) is calculated using the following formula AG = ([Na+ + K+] - [Cl- + HCO,]). In our illustrative case, the anion gap was 28, indicating severe metabolic acidosis. 

Acute intoxication with phenylbutazone is dominated by metabolic acidosis, which can progress to coma, seizures, hypotension, shock, and oliguria. Kidney and liver reactions, acute bone marrow depression, and acute perforation of peptic ulcer have all been described (5,11,35). 

In another case of acute systemic allergy to quinine, which mimicked septic shock, with little hemolysis or renal involvement, the patient presented twice with a virtually identical clinical picture sudden fever, rigors, and back pain, followed by hypotension, metabolic acidosis, granulocytopenia, and disseminated intravascular coagulation. On each occasion chnical and laboratory indices recovered spontaneously within 36 hours. A retrospective analysis of the patient s serum showed the presence of neutrophil-specific, quinine-dependent antibodies. 

Severe adverse drug reactions with trimethoprim and co-trimoxazole are rare (12-14). This also applies to children (15). The adverse effects of co-trimoxazole correspond to those expected from a sulfonamide (16). In HIV-infected patients, adverse effects of co-trimox-azole are more frequent and more severe (17-19). Hematological disturbances due to co-trimoxazole include mild anemia, leukopenia, and thrombocytopenia, which may be due to folic acid antagonism. Serious metabolic disturbances that are associated with trimethoprim include hyperkalemia and metabolic acidosis. Trimethoprim can cause hypersensitivity reactions. However, with co-trimoxazole, the sulfonamide is generally believed to be more allergenic (12). Generalized skin reactions predominate. Other effects, such as anaphylactic shock, are extremely rare (20-22). Carcinogenicity due to trimethoprim or co-trimoxazole has not been reported. 

Bjerneroth G, Sammeli 0, Li Y-C et al 1994 Effects of alkaline buffers on cytoplasmic pH in lymphocytes. Critical Care Medicine 22 1550-1556 Boilaert P E, Levy B, Nace L et al 1995 Hemodynamic and metabolic effects of rapid correction of hypophosphatemia in patients with septic shock. Chest 107 1698-1701 Bonagura J D, Reef V B 1998 Cardiovascular diseases. In Reed S M, Bayly W M (eds) Equine internal medicine. Saunders, Philadelphia, PA, pp. 290-370 Bonventre J V, Cheung J Y 1985 Effects of metabolic acidosis on viability of cells exposed to anoxia. 

Lactic acidosis occurs in two clinical settings (1) type A (hypoxic), associated with decreased tissue oxygenation, such as shock, hypovolemia, and left ventricular failure and (2) type B (metabolic), associated with disease (e.g., diabetes melUtus, neoplasia, liver disease), drugs and/or toxins (e.g., ethanol, methanol, and salicylates), or inborn errors of metabolism (e.g., methylmalonic aciduria, propionic acidemia, and fatty acid oxidation defects). Lactic acidosis is not uncommon and occurs in approximately 1% of hospital admissions. It has a mortality rate greater than 60%, which approaches 100% if hypotension is also present. Type A is much more common. 

A 55-year-old woman and a 34-year-old man ingested, with suicidal intent, an unknown amount of what was reported to have been formalin (Koppel et al. 1990). The female patient was found in a coma and admitted to the hospital with shock (systolic blood pressure 50 mm Hg), respiratory insufficiency, and metabolic acidosis. The male patient, who had a history of alcohol abuse, was also hospitalized with shock (systolic blood pressure 60 mm Hg), respiratory insufficiency, and metabolic acidosis. Both patients underwent hemodialysis and hemofiltration treatment. Analysis of the formaldehyde samples ingested by both patients showed no evidence that these products contained methanol, although it was expected to have been detected. A chemical-toxicological screening indicated that no drugs other than fonnaldehyde had been ingested neither methanol or ethanol were detected in blood samples. Three... 

Patients with systemic symptoms (e.g., shock, coma, or gross gastrointestinal bleeding or metabolic acidosis) should receive deferoxamine as soon as possible. If the serum iron concentration exceeds 500 mcg/dL, deferoxamine is also indicated because serious systemic toxicity is hkely. Its use is less clear in patients with serum iron concentrations in the range of350-500 mcg/dL because many of these patients do not develop systemic symptoms. ... 

Hatherill M, Waggie Z, Purves L, et al. Mortahty and the nature of metabolic acidosis in children with shock. Int Care Med 2003 29 286-291. 

Mixed respiratory and metabolic acidosis may develop in patients with cardiorespiratory arrest, in those with chronic lung disease who are in shock, and in metabolic acidosis patients who develop respiratory failure. This mixed disorder should be treated by responding to both the respiratory and metabolic acidosis. Improved oxygen delivery must be initiated to improve hypercarbia and hypoxia. Mechanical ventilation may be needed to reduce PaC02. During the initial stage of therapy, appropriate amounts of alkali should be given to reverse the metabolic acidosis (see section on treatment of metabolic acidosis earlier in this chapter). 

Cardiovascular effects. In severe cases, extensive tissue third spacing of fluids combined with fluid loss from gastroenteritis may lead to hypotension, tachycardia, shock, and death. Metabolic acidosis and rhabdomyoly-sis may be present. After a delay of 1-6 days, there may be a second phase of congestive cardiomyopathy, cardiogenic or noncardiogenic pulmonary edema, and isolated or recurrent cardiac arrhythmias. Prolongation of the QT interval may be associated with torsade de pointes ventricular arrhythmia. 

B. Dermal. Industrial workers handling bulk sodium azide experienced headache, nausea, faintness, and hypotension, but it is unclear whether the exposure occurred via dermal absorption or inhalation. An explosion of a metal waste drum containing a 1% sodium azide solution caused bums over a 45% body surface area and led to typical azide toxicity with a time course similar to oral ingestion coma and hypotension developed within 1 hour followed by refractory metabolic acidosis, shock, and death 14 hours later. 

C. This may be followed by an abrupt relapse with coma, shock, seizures, metabolic acidosis, coagulopathy, hepatic failure, and death. Yersinia enterocolit-ica sepsis may occur. 

The administration of bicarbonate is to be used with cautioa The indiscriminate use of bicarbonate is particularly dangerous in resuscitation of patients with metabolic acidosis as a concomitant of hypovolaemic shock lactic acid itself is innocuous and is readily removed by the liver as soon as the perfusion of the tissues is re-established. If administration of bicarbonate causes alkalosis and shifts the oxygen dissociation curve to the left, there is interference with oxygen unloading at the cellular level in tissues which are already hypoxic. Treatment of metabolic acidosis by bicarbonate therapy is reserved for situations in which partial correction of the pH is needed to restore cardiac function, which is depressed by acidaemia as described in Chapter 4. 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

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