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Chapter: Clinical Anesthesiology: Perioperative & Critical Care Medicine: Critical Care

Septic Shock

The SCCM/ESICM/ACCP/ATS/SIS Consensus Conference defined septic shock as sepsis asso-ciated with hypotension (systolic blood pressure <90 mm Hg, mean arterial pressure <60 mm Hg, or systemic blood pressure <40 mm Hg from baseline) despite adequate fluid resuscitation.



The SCCM/ESICM/ACCP/ATS/SIS Consensus Conference defined septic shock as sepsis asso-ciated with hypotension (systolic blood pressure <90 mm Hg, mean arterial pressure <60 mm Hg, or systemic blood pressure <40 mm Hg from baseline) despite adequate fluid resuscitation. Septic shock is usually characterized by inadequate tissue perfusion and widespread cellular dysfunction. In contrast to other forms of shock (hypovolemic, cardiogenic, neurogenic, or anaphylactic), cellular dysfunction in septic shock is not necessarily related to the hypo-perfusion. Instead, metabolic blocks at the cellu-lar and microcirculation levels may contribute to impaired cellular oxidation.



An infectious process that induces a severe or pro-tracted SIRS can result in septic shock. In hospital-ized patients septic shock most commonly follows gram-negative infections in either the genitourinary tract or the lungs, but identical presentations can be seen with other pathogens. In up to 50% of cases of severe sepsis no organisms can be cultured from blood. Hypotension is due to a decreased circulating intravascular volume resulting from a diffuse capil-lary leak. Patients may also have myocardial depres-sion. Activation of platelets and the coagulation cascade can lead to the formation of fibrin-platelet aggregates, which further compromise tissue blood flow. Hypoxemia from ARDS accentuates tissue hypoxia. The release of vasoactive substances and formation of microthrombi in the pulmonary circu-lation increase pulmonary vascular resistance.

Hemodynamic Subsets


The circulation in patients with septic shock is often described as either hyperdynamic or hypodynamic. In reality, both represent the same process, but their expression depends on preexisting cardiac function and intravascular volume and the patient’s response. Systemic venodilation and transudation of fluid into tissues result in relative hypovolemia


in patients with sepsis. Hyperdynamic septic shock is characterized by normal or elevated cardiac out-put and profoundly reduced systemic vascular resis-tance. Decreased myocardial contractility is often demonstrable by echocardiography even in hyper-dynamic patients with increased cardiac output. Mixed venous oxygen saturation is characteristically increased in the absence of hypoxemia and likely reflects the increased cardiac output and the cellular metabolic defect in oxygen utilization.

It used to be accepted wisdom that hypody-namic septic shock, characterized by decreased car-diac output with low or normal systemic vascular resistance, was usually seen later in the course of shock. This view is false; hypodynamic shock often occurs early in the course of septic shock. It is more likely to be seen in severely hypovolemic patients and in those with underlying cardiac disease. Myo-cardial depression is prominent. Mixed venous oxygen saturation is reduced in these patients, and pulmonary hypertension is often prominent. Eleva-tion of pulmonary vascular resistance widens the normal pulmonary artery diastolic-to-wedge pres-sure gradient; large gradients have been associated with a higher mortality rate. The increase in pulmo-nary vascular resistance may contribute to right ven-tricular dysfunction.

Clinical Manifestations


Manifestations of septic shock appear to be pri-marily related to host response rather than the infective agent. Septic shock classically presents with an abrupt onset of chills, fever, nausea (and often vomiting), decreased mental status, tachy-pnea, hypotension, and tachycardia. The patient may appear flushed and feel warm (hyperdynamic) or pale with cool and often cyanotic extremities (hypodynamic). In old, debilitated patients and in infants, the diagnosis often is less obvious and hypothermia may be seen.


Leukocytosis with a leftward shift to premature cell forms is typical, but leukopenia can be seen with overwhelming sepsis and is an ominous sign. Pro-gressive metabolic acidosis (usually lactic acidosis) is typically partially compensated by a concomitant respiratory alkalosis. Elevated lactate levels reflect both increased production resulting from poor tis-sue perfusion and decreased uptake by the liver and kidneys. Hypoxemia may herald the onset of ARDS. Oliguria due to the combination of hypovolemia, hypotension, and a systemic inflammatory insult will often progress to kidney failure. Elevations in serum aminotransferases and bilirubin are due to hepatic dysfunction. Insulin resistance is uniformly present and produces hyperglycemia. Thrombocyto-penia is common and is often an early sign of sepsis. Laboratory evidence of disseminated intravascular coagulation (DIC) is often present but is rarely asso-ciated with a bleeding diathesis. The latter responds only to control of the sepsis. Stress ulceration of gas-tric mucosa is common. Respiratory and kidney fail-ure are the leading causes of death in septic patients.

Neutropenic patients (absolute neutrophil count 500/µL) may develop macular or papular lesions that can ulcerate and become gangrenous (ecthyma gangrenosum). These lesions are com-monly associated with Pseudomonas septicemia but can be caused by other organisms. Perirectal abscesses can develop very quickly in neutropenic patients with few external signs; conscious patients may complain only of perirectal pain.



Septic shock is a medical emergency that requires immediate intervention. Treatment is threefold:

control and eradication of the infection by appro-priate and timely intravenous antibiotics, drainage of abscesses, debridement of necrotic tissues, and removal of infected foreign bodies; (2) maintenance of adequate perfusion with intravenous fluids and inotropic and vasopressor agents; and (3) supportive treatment of complications such as ARDS, kidney failure, gastrointestinal bleeding, and DIC.

Antibiotic treatment usually is initiated before pathogens are identified but only after adequate cul-tures are obtained (commonly, blood, urine, wounds, and sputum). Pending the results of cultures and tests of antibiotic sensitivity, combination therapy with two or more antibiotics is generally indicated. Typi-cally, the combination of a penicillin/β-lactamase inhibitor or third-generation cephalosporin with an aminoglycoside is used. The choice depends on which organisms are seen with the greatest frequency in one’s medical center. Additional diagnostic stud-ies may be indicated (eg, thoracentesis, paracentesis, lumbar puncture, or imaging), depending on the history and physical examination.

Empiric antibiotic therapy in immunocompro-mised patients should be based on pathogens that are generally associated with the immune defect (see Table 57–11). Vancomycin is added if intravascular catheter-related infection is suspected. Clindamy-cin or metronidazole may be given to neutrope-nic patients if a rectal abscess is suspected. Many clinicians initiate therapy for a presumed fungal infection when an immunocompromised patient continues to experience fever despite antibiotic therapy. Granulocyte colony-stimulating factor or granulocyte–macrophage colony-stimulating factor may be used to shorten the period of neutropenia; granulocyte transfusion may occasionally be used in refractory gram-negative bacteremia. Diffuse interstitial infiltrates on a chest radiograph may sug-gest unusual bacterial, parasitic, or viral pathogens; many clinicians initiate empiric therapy with trim-ethoprim-sulfamethoxazole and erythromycin in such instances. Nodular infiltrates on a radiograph suggest a fungal pneumonia and may warrant anti-fungal therapy. Antiviral therapy should be consid-ered in septic patients who are more than 1 month post–bone marrow or solid organ transplantation.


In general, therapy should follow the most recent SCCM/ESICM “surviving sepsis” guidelines. The presence of inadequate perfusion is determined by measurement of blood lactate. “Goal-directed” hemodynamic support is also recommended by many groups. Tissue oxygenation and perfusion are supported with oxygen, intravenous fluids, inotro-pes, and vasopressors. Central venous pressure is maintained at greater than 8 mm Hg and central venous oxygen saturation is maintained at greater than 70%. Packed red blood cell transfusions are given to keep hemoglobin levels greater than 8 g/dL, especially when central venous pressure and cen-tral venous oxygen saturation are below targets. Marked “third-spacing” has long been regarded as characteristic of septic shock, but currently there is debate regarding the existence of the third space and the administration of large volumes of intravenous fluid as to which is cause and which is effect. Colloid solutions more rapidly restore intravascular volume compared with crystalloid solutions but other-wise offer no proven additional benefit. Vasopres-sor therapy is generally initiated if hypotension (mean arterial pressure <65 mm Hg) or elevated blood lactate levels persist following administra-tion of intravenous fluids. Suggested choices arenorepinephrine or dopamine; other positive ino-tropic drugs (eg, dobutamine) are indicated only when the SVO2 falls below 70% despite fluids and vasopressor therapy. Patients with persisting eleva-tions of lactate or persisting low central venous oxy-gen saturations, despite treatment, should receive a week-long course of steroids (200–300 mg/d of hydrocortisone or the equivalent in divided doses or by infusion). Blood glucose should be controlled with a target value of less than 180 mg/dL. In patients with hypotension that is refractory to norepineph-rine plus dopamine or dobutamine, vasopressin may be administered to improve blood pressure. Severe acidosis may decrease the efficacy of inotropes and should therefore generally be corrected (pH > 7.20) with bicarbonate or THAM infusion in patients with refractory hypotension and lactic acidosis. “Renal” doses of dopamine or fenoldopam may increase uri-nary output but have not been shown to improve or protect kidney function or patient outcomes. Clinical trials of naloxone, opsonins (fibronectin), inhibitors of the coagulation cascade (drotrecogin alfa), and monoclonal antibodies directed against lipopolysaccharide in septic shock have been disappointing.

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