Septic Shock
Low systemic vascular resistance and an elevated cardiac output characterize septic shock. The disorder is thought to occur in response to infections that release microbes or one of the immune mediators.
Septic shock is usually a complication of another disorder or invasive procedure and has a mortality as high as 25%.
Causes
Any pathogenic organism can cause septic shock. Gram-negative bacteria, such as Escherichia coli, Klebsiella pneumoniae, Serratia, Enterobacter, and Pseudomonas, rank as the most common causes and account for up to 70% of all cases. Opportunistic fungi cause about 3% of cases. Rare causative organisms include mycobacteria and some viruses and protozoa.
Many organisms that are normal flora on the skin and in the intestines are beneficial and pose no threat. But when they spread throughout the body by way of the bloodstream (gaining entry through any alteration in the body’s normal defenses or through artificial devices that penetrate the body, such as I.V., intra-arterial, and urinary catheters and knife or bullet wounds), they can progress to overwhelming infection unless body defenses destroy them.
Initially, these defenses activate chemical mediators in response to the invading organisms. The release of these mediators results in low systemic vascular resistance and increased cardiac output. Blood flow is unevenly distributed in the microcirculation, and plasma leaking from capillaries causes functional hypovolemia. Eventually, cardiac output falls, and poor tissue perfusion and hypotension cause multisystem organ failure and death.
Septic shock can occur in any person with impaired immunity, but elderly people are at greatest risk. About two-thirds of septic shock cases occur in hospitalized patients, most of whom have underlying diseases. Those at high risk include patients with burns, diabetes mellitus, immunosuppression, malnutrition, stress, excessive antibiotic use, and chronic cardiac, hepatic, or renal disorders. Also at risk are patients who have had invasive diagnostic or therapeutic procedures, surgery, or traumatic wounds.
Complications
In septic shock, complications include disseminated intravascular coagulation, renal failure, heart failure, GI ulcers, and abnormal liver function. Carriers of the TNF2 polymorphism in the tumor necrosis factor alpha (TNF-alpha) gene promoter may have an increased susceptibility to septic shock and may also be more likely to die if septic shock develops.
Assessment
The patient’s history may include a disorder or treatment that can cause immunosuppression, or it may include a history of invasive tests or treatments, surgery, or trauma. At onset, the patient may have fever and chills, although 20% of patients may be hypothermic.
The patient’s signs and symptoms will reflect either the hyperdynamic (warm) phase of septic shock or the hypodynamic (cold) phase.
The hyperdynamic phase is characterized by increased cardiac output, peripheral vasodilation, and decreased systemic vascular resistance. The patient’s skin may appear pink and flushed. His altered level of consciousness is reflected in agitation, anxiety, irritability, and shortened attention span. Respirations are rapid and shallow. Urine output is below normal.
Palpation of peripheral pulses may detect a rapid, full, bounding pulse. The skin may feel warm and dry. Blood pressure may be normal or slightly elevated.
The hypodynamic phase is characterized by decreased cardiac output, peripheral vasoconstriction, increased systemic vascular resistance, and inadequate tissue perfusion. The patient’s skin may appear pale and possibly cyanotic. Peripheral areas may be mottled. His level of consciousness may be decreased; obtundation and coma may be present. Respirations are rapid and shallow, and urine output may be less than 25 ml/hour or absent.
Palpation of peripheral pulses may reveal no pulse or a rapid pulse that’s weak or thready. Peripheral pulses may also be irregular if arrhythmias are present. The skin may feel cold and clammy.
Auscultation of blood pressure may reveal hypotension, usually with a systolic pressure below 90 mm Hg or 50 to 80 mm Hg below the patient’s previous level. Auscultation of the lungs may reveal crackles or rhonchi if pulmonary congestion is present.
The pulmonary artery wedge pressure is likely to be reduced or normal, and cardiac output is almost always moderately to severely increased or normal. Rarely, cardiac output is decreased.