Distributive Shock Clinical Presentation
- Author: Klaus-Dieter Lessnau, MD, FCCP; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more...
Patients with shock frequently present with tachycardia, tachypnea, hypotension, altered mental status changes, and oliguria.
Patients with septic shock or systemic inflammatory response syndrome (SIRS) may have prior symptoms that suggest infection or inflammation of the respiratory tract, urinary tract, or abdominal cavity.
Septic shock occurs frequently in hospitalized patients with risk factors such as indwelling catheters or venous access devices, recent surgery, or immunosuppressive therapy.
Patients with anaphylaxis commonly have recent iatrogenic (drug) or accidental (bee sting) exposure to an allergen and coexisting respiratory symptoms, such as wheezing and dyspnea, pruritus, or urticaria.
Staphylococcal toxic shock syndrome (TSS) is still observed most commonly in women who are menstruating, but it is also associated with recent soft-tissue injury, cutaneous infections, postpartum and cesarean delivery, wound infections, pharyngitis, and focal staphylococcal infections, such as abscess, empyema, pneumonia, and osteomyelitis. Patients often have a history of influenzalike illness (fever, arthralgias, myalgias) and a desquamating rash.
Pancreatitis may be another cause of distributive shock; expect symptoms of abdominal pain that radiate to the back, as well as nausea and vomiting. Burns also have been described as a cause of distributive shock.
Adrenal insufficiency as a cause of shock should be considered in any patient with hypotension who lacks signs of infection, cardiovascular disease, or hypovolemia.
Long-term treatment with corticosteroids may result in inadequate response of the adrenal axis to stress, such as infection, surgery, or trauma, and subsequent onset or worsening of shock.
If the clinical picture is consistent with adrenal insufficiency in a person without this diagnosis, consider that this could be the first presentation of this disorder.
There is a high incidence of adrenal insufficiency in critically ill patients infected with the human immunodeficiency virus (HIV), although this incidence varies with the criteria used to diagnose adrenal insufficiency.
Cardinal features of distributive shock include the following:
Change in mental status
Heart rate - Greater than 90 beats per minute (note that heart rate elevation is not evident if the patient is on a beta blocker)
Hypotension - Systolic blood pressure less than 90 mm Hg or a reduction of 40 mm Hg from baseline
Respiratory rate - Greater than 20 breaths per minute
Extremities - Frequently warm, with bounding pulses and increased pulse pressure (systolic minus diastolic blood pressure) in early shock; late shock may present as critical organ dysfunction
Hyperthermia - Core body temperature greater than 38.3°C (101°F)
Hypothermia - Core body temperate less than 36°C (96.8°F)
Pulse oximetry - Relative hypoxemia
Decreased urine output
Clinical symptoms of the underlying infections found in distributive shock include the following:
Pneumonia - Dullness to percussion, rhonchi, crackles, bronchial breath sounds
Urinary tract infection - Costovertebral angle tenderness, suprapubic tenderness, dysuria and polyuria
Intra-abdominal infection or acute abdomen - Focal or diffuse tenderness to palpation, diminished or absent bowel sounds, rebound tenderness
Gangrene or soft-tissue infection - Pain out of proportion to lesion, skin discoloration and ulceration, desquamating rash, areas of subcutaneous necrosis
Anaphylaxis is characterized by the following clinical symptoms:
TSS is characterized by the following clinical symptoms:
Diffuse rash with desquamation on the palms and soles over a subsequent 1-2 weeks
Hypotension (may be orthostatic) and evidence of involvement of 3 other organ systems
Streptococcal TSS more frequently presents with focal soft-tissue inflammation and is less commonly associated with diffuse rash. Occasionally, it can progress explosively within hours.
Adrenal insufficiency is characterized by the following clinical symptoms:
Hyperpigmentation of skin, oral, vaginal, and anal mucosal membranes may be present in chronic adrenal insufficiency.
In acute or acute-on-chronic adrenal insufficiency brought on by physiologic stress, hypotension may be the only physical sign.
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|Diagnosis||Pulmonary Capillary Wedge Pressure||Cardiac Output|
|Extracardiac obstructive shock
1. Pericardial tamponade†
2. Pulmonary embolism
Normal or decreased
1. Septic shock
2. Anaphylactic shock
|Normal or decreased
Normal or decreased
|Increased or normal
Increased or normal
|*In cardiogenic shock due to a mechanical defect, such as mitral regurgitation, forward cardiac output is reduced, although the measured cardiac output may be unreliable. Large V waves are commonly observed in the pulmonary capillary wedge tracing in mitral regurgitation.
†The hallmark finding is equalization of right atrial mean, right ventricular end-diastolic, pulmonary artery (PA) end-diastolic, and pulmonary capillary wedge pressures.
|Drug||Dose||Principal Mechanism||Cardiac Output||Blood Pressure||SVR|
|Dobutamine||2-20 mcg/kg/min||Beta 1||++||+||+|
|5-10 mcg/kg/min||Beta 1, dopamine||++||+||+|
|Epinephrine (low dose)||0.06-0.20 mcg/kg/min||Beta 1, beta 2 >alpha||++||+||+|
|Inotropic agents and vasoconstrictors|
|Dopamine (high dose)||>10 mcg/kg/min||Alpha, beta 1, dopamine||++||++||+|
|0.21-0.42 mcg/kg/min||Alpha >beta 1, beta 2||++||++||+|
|Norepinephrine||0.02-0.25 mcg/kg/min||Alpha >beta 1, beta 2||+||++||++|
|Vasopressin||0.10-0.40 U/min||V1 receptor||+||+||++|
(very low dose)
|Milrinone||0.4-0.6 mcg/kg/min after loading dose; 50 mcg/kg bolus over 5 min||Phosphodiesterase inhibitor||+||+/-||-|
|Alpha and beta refer to agonist activity at these adrenergic receptor sites.
Beta 1-adrenergic effects are inotropic and increase contractility.
Beta 2-adrenergic effects are chronotropic.
|Suspected Source||Recommended Antibiotic Therapy||Alternative Therapy|
|No source evident in a healthy host||Third-generation cephalosporin, eg, ceftriaxone 2 g IV q12h, ceftizoxime, ceftazidime||Nafcillin and aminoglycoside, imipenem, piperacillin/tazobactam|
|No source evident in an immunocompromised host||Ceftazidime 2 g IV q8h plus aminoglycoside||Imipenem or piperacillin/tazobactam plus aminoglycoside|
|No source evident in a user of intravenous drugs||Nafcillin 2 g IV q4h plus aminoglycoside||Vancomycin plus aminoglycoside, ceftazidime, imipenem, or piperacillin/tazobactam|
|Bacterial pneumonia, community acquired||Ceftriaxone 2 g IV q12-24 h plus macrolide||Levofloxacin 750mg IV q24h, cotrimoxazole or imipenem plus macrolide|
|Bacterial pneumonia, hospital acquired||Piperacillin/tazobactam 4.5 g IV q6h plus aminoglycoside, plus levofloxacin 750 mg IV q24h||Imipenem plus aminoglycoside, plus macrolide|
|Urinary tract infection||Ampicillin 2 g IV q4h plus aminoglycoside||Fluoroquinolone or third-generation cephalosporin plus aminoglycoside|
|Mixed aerobic and anaerobic abdominal sepsis, aspiration pneumonia, pelvic infection, and necrotizing cellulitis||Third-generation cephalosporin or ampicillin 2 g IV q4h plus aminoglycoside plus clindamycin 600 mg IV q8h or metronidazole 500 mg IV q6h||Fluoroquinolone plus clindamycin, imipenem, piperacillin/tazobactam|
|Meningitis||Ceftriaxone 2 g IV q12h plus vancomycin||Meropenem plus vancomycin, chloramphenicol plus cotrimoxazole plus vancomycin|
|Cellulitis/erysipelas||Nafcillin 2 g IV q4h||Cefazolin, vancomycin, clindamycin|
|Toxic shock syndrome (TSS) or streptococcal necrotizing fasciitis||Clindamycin 600 mg IV q8h||Cephalosporin, vancomycin, nafcillin|