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Septic Shock (Endotoxic Shock): Medical Implications, Clinical Manifestations And Diagnosis

Updated on March 22, 2014

Clinical Care Of A Septic Shock Patient

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Septic Shock

The importance of septic shock as a life- threatening emergency in several infections has been recognized in recent times. In most cases, endotoxins of Gram- negative bacilli are responsible. Probably, prevalence of septic shock has increased among hospitalized patients in the past two decades. Common organisms are E. Coli, Klebsiella, proteus, enterobacter and pseudomonas. Less frequently, shock is caused by bacteriodes, Mima herella, salmonella and serratia. Gram- positive organisms like clostridia, staphylococci and streptococci and Gram- negative cocci such as meningococci may sometimes cause septicemia and shock. Viruses, rickettsiae or fungi may be isolated at times. Septic shock is more frequent in men than women. Several cases of toxic shock syndrome have been described in women caused by toxigenic strains of staphylococci contaminating vaginal tampons. Debilitating disorders such as diabetes, cirrhosis and leukemia and use of immunosuppressant drugs (corticosteroids) are associated with higher incidence. Extensive burns, manipulation of infected tissues and surgery may precipitate septic shock.

Vascular phenomena contribute to the development of shock. The endotoxin depresses myocardial function and widespread cellular and tissue injury results. In most patients with septic shock, the syndrome of disseminated intravascular coagulation (DIC) sets in. Respiratory failure is a frequent cause of death. The respiratory lesions have been collectively termed the “shock- lung syndrome”. Oliguria occurs early and is probably caused by inadequate renal perfusion and a direct toxic effect on the kidneys. Acute renal failure may develop.

Managing Septic Shock In Newborns

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Clinical Presentations And Diagnosis Of Septic Shock

Clinical Manifestations

Classical features of shock such as hypotension, weak thread pulse, cold clammy skin, tachycardia, tachypnea, peripheral cyanosis, oliguria and alteration of the sensorium are all present. This may be preceded by fever. There may be marked dehydration, electrolyte imbalabce, acidosis, and impaired renal function. In a small proportion of patients, a warm- shock picture may predominate. This is characterized by hypotension, warm pink skin, minimal alteration of sensorium and adequate urine output. This stage is transient and it soon progresses to the more common form of vasoconstrictive shock. Not infrequently, the blood pressure may be normal in the presence of vasoconstrictive shock. Marked tachypnea occurs due to a direct effect of endotoxin on the respiratory center and this may result in respiratory alkalosis. With the passage of time, respiratory alkalosis gives way to metabolic acidosis. Cardiac failure, respiratory failure and coma supervene. Death is caused by pulmonary edema, tissue anoxia, cardiac arrhythmias or disseminated intravascular coagulation.

Diagnosis

Though in the majority of cases, the clinical picture of shock is very evident, in a few the findings are bizarre, particularly in old debilitated patients. Septic shock should be suspected in the presence of unexplained hypotension, increasing confusion; disorientation or hyperventilation. Some patients may not develop fever. On the contrary, they may be hypothermic and such cases may be missed. Presence of jaundice should suggest cholangitis, toxic hepatitis or disseminated intravascular coagulation.

© 2014 Funom Theophilus Makama

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