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Painless persistent edema of one or both lower extremities, primarily in young women Pitting edema, which rarely becomes brawny and non-pitting Ulceration, varicosities, and stasis pigmentation do not occur There may be episodes of lymphangitis and cellulitis
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With aggressive treatment, including pneumatic compression devices, good relief of symptoms can be achieved The long-term outlook is dictated by the associated conditions and avoidance of recurrent cellulitis
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Tiwari A et al Differential diagnosis, investigation, and current treatment of lower limb lymphedema Arch Surg 2003 Feb; 138(2):152 61 [PMID: 12578410]
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The underlying mechanism in lymphedema is impairment of the lymph flow from an extremity When lymphedema
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Table 12 1 Classification of shock by mechanism and common causes
Hypovolemic shock Loss of blood (hemorrhagic shock) External hemorrhage Trauma Gastrointestinal tract bleeding Internal hemorrhage Hematoma Hemothorax or hemoperitoneum Loss of plasma Burns Exfoliative dermatitis Loss of fluid and electrolytes External Vomiting Diarrhea Excessive sweating Hyperosmolar states (diabetic ketoacidosis, hyperosmolar nonketotic coma) Internal ( third spacing ) Pancreatitis Ascites Bowel obstruction Cardiogenic shock Dysrhythmia Tachyarrhythmia Bradyarrhythmia Pump failure (secondary to myocardial infarction or other cardiomyopathy) Acute valvular dysfunction (especially regurgitant lesions) Rupture of ventricular septum or free ventricular wall Obstructive shock Tension pneumothorax Pericardial disease (tamponade, constriction) Disease of pulmonary vasculature (massive pulmonary emboli, pulmonary hypertension) Cardiac tumor (atrial myxoma) Left atrial mural thrombus Obstructive valvular disease (aortic or mitral stenosis) Distributive shock Septic shock Anaphylactic shock Neurogenic shock Vasodilator drugs Acute adrenal insufficiency Reproduced, with permission, from Stone CK, Humphries RL (editors) Current Emergency Diagnosis & Treatment, 5th ed p 193 McGraw-Hill, 2004
Hypotension, tachycardia, oliguria, altered mental status Peripheral hypoperfusion and impaired oxygen delivery
General Considerations
Shock occurs when the rate of arterial blood flow is inadequate to meet tissue metabolic needs This results in regional hypoxia and subsequent lactic acidosis from anaerobic metabolism in peripheral tissues as well as eventual end-organ damage and failure
Classification (Table 12 1)
A Hypovolemic Shock
Hypovolemic shock results from decreased intravascular volume secondary to loss of blood or fluids and electrolytes The etiology may be suggested by the clinical setting (eg, trauma) or by signs and symptoms of blood loss (eg, gastrointestinal bleeding) or dehydration (eg, vomiting or diarrhea) Compensatory vasoconstriction may transiently maintain the blood pressure but unreplaced losses of over 15% of the intravascular volume can result in hypotension and progressive tissue hypoxia
B Cardiogenic Shock
Cardiogenic shock results from pump failure This may be related to myocardial infarction, cardiomyopathy, myocardial contusion, valvular incompetence or stenosis, or arrhythmias See 10
C Obstructive Shock
Cardiac tamponade, tension pneumothorax, and massive pulmonary embolism can cause an acute decrease in cardiac output resulting in shock These are medical emergencies requiring prompt diagnosis and treatment
D Distributive Shock
Distributive or vasodilatory shock has many causes including sepsis, anaphylaxis, systemic inflammatory response syndrome (SIRS) produced by severe pancreatitis or burns, or acute adrenal insufficiency The reduction in systemic vascular resistance results in inadequate cardiac output and tissue hypoperfusion despite normal circulatory volume 1 Septic shock Sepsis is the most common cause of distributive shock and carries a high mortality rate of 30 87% Sepsis is typically secondary to gram-negative bacteremia (such as Escherichia coli, Klebsiella, Proteus, and
Pseudomonas) and less often due to gram-positive cocci and gram-negative anaerobes (Bacteroides) Risk factors include extremes of age, diabetes, immunosuppression, and history of a recent invasive procedure 2 Neurogenic shock Neurogenic shock is caused by traumatic spinal cord injury or effects of an epidural or spinal anesthetic This results in loss of sympathetic tone with a reduction in systemic vascular resistance and hypotension without a compensatory tachycardia Reflex vagal parasympathetic stimulation evoked by pain, gastric dilation, or fright may simulate neurogenic shock, producing hypotension, bradycardia, and syncope
Blood Vessels & Lymphatics
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Clinical Findings
Hypotension in adults is traditionally defined as a systolic blood pressure of 90 mm Hg or less or a mean arterial pressure of less than 60 65 mm Hg but must be evaluated relative to the patient s normal blood pressure A drop in systolic pressure of more than 10 20 mm Hg and an increase in pulse of more than 15 beats per minute with positional change suggests depleted intravascular volume However, blood pressure is often not the best indicator of organ perfusion because compensatory mechanisms, such as increased heart rate, contractility and, vasoconstriction can occur to prevent hypotension Patients often have cool or mottled extremities and weak or thready peripheral pulses Splanchnic vasoconstriction may lead to oliguria, bowel ischemia, and hepatic dysfunction, which can ultimately result in multiorgan failure Mentation may be normal or patients may become restless, agitated, confused, lethargic, or comatose as a result of inadequate perfusion of the brain Consequently, intubation and mechanical ventilation may be required to protect the patient s airway Hypovolemic shock is evident when signs of hypoperfusion, such as oliguria, altered mental status, and cool extremities, are present Jugular venous pressure is low, and there is a narrow pulse pressure indicative of reduced stroke volume TEE shows reduced left ventricular filling Rapid replacement of fluids restores tissue perfusion and often confirms the diagnosis In cardiogenic shock, there are signs of global hypoperfusion with oliguria, altered mental status, and cool extremities Jugular venous pressure is elevated TEE shows an enlarged left ventricle There may be evidence of pulmonary edema in the setting of left sided heart failure and evidence of ECG changes In obstructive shock, the central venous pressure may be elevated but the TEE shows reduced LV filling Pericardiocentesis or pericardial window, chest tube placement, or catheter-directed thrombolytic therapy can be lifesaving In distributive shock, signs include hyperdynamic heart sounds, warm extremities, and a wide pulse pressure indicative of large stroke volume Fluid resuscitation may have little effect on blood pressure, urinary output, or mentation Septic shock is diagnosed when there is clinical evidence of infection in the setting of persistent hypotension and evidence of organ hypoperfusion, such as in lactic acidosis, decreased urinary output, or altered mental status despite volume resuscitation
ing and assessment of hemodynamic parameters such as blood pressure and heart rate Cardiac monitoring can detect myocardial ischemia requiring cardiac catheterization or malignant arrhythmias, which can be treated by standard advanced cardiac life support (ACLS) protocols Unresponsive or minimally responsive patients should immediately be given 1 ampule of 50% dextrose intravenously and 2 mg of naloxone intravenously or intramuscularly An arterial line should be placed for continuous blood pressure measurement, and a Foley catheter should be inserted to monitor urinary output Blood specimens should be evaluated for complete blood count, electrolytes, glucose, arterial blood gas determinations, coagulation parameters, typing and cross-matching, and bacterial cultures
B Central Venous Pressure (CVP) or Pulmonary Capillary Wedge Pressure (PCWP)
Early consideration is given to placement of a central line or pulmonary artery catheter for hemodynamic pressure measurements A pulmonary artery catheter can be helpful in distinguishing cardiogenic and septic shock and in monitoring the effects of volume resuscitation or pressor medications Because of the attendant risks associated with pulmonary artery catheters (such as infection, arrhythmias, vein thrombosis, and pulmonary artery rupture), the value of the information they might provide must be carefully weighed in each patient Pulmonary artery catheters are most useful in the management of patients with cardiogenic shock In patients with other types of shock, a central venous line may be adequate Central lines also can provide a measurement of the central venous oxygen saturation In general, a central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP) under 5 mm Hg suggests hypovolemia and over 18 mm Hg suggests volume overload, cardiac failure, tamponade, or pulmonary hypertension A cardiac index < 2 L/min/m2 indicates a need for inotropic support A high cardiac index > 4 L/min/m2 in a hypotensive patient is consistent with early septic shock The systemic vascular resistance is low (< 800 dyness/cm 5) in sepsis and neurogenic shock and high (< 1500 dynes/cm 5) in hypovolemic and cardiogenic shock Treatment is directed at maintaining a CVP of 8 12 mm Hg, and mean arterial pressure of 65 90 mm Hg, a cardiac index of 2-4 L/min/m2, and a central venous oxygen saturation of greater than 70%
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