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  • Cited by 2
  • Edited by Kaushal Shah, Department of Emergency Medicine, Mount Sinai School of Medicine, New York, Jarone Lee, Department of Emergency Medicine, Massachusetts General Hospital, Boston, Kamal Medlej, American University of Beirut, Scott D. Weingart, Department of Emergency Medicine, Mount Sinai School of Medicine, New York
Publisher:
Cambridge University Press
Online publication date:
November 2013
Print publication year:
2013
Online ISBN:
9781139523936

Book description

Acute resuscitation and care of unstable and critically ill patients can be a daunting experience for all trainees in the emergency department or the intensive care unit. The practical, easy-to-read and evidence-based information in Practical Emergency Resuscitation and Critical Care will help all physicians understand and begin management of these patients. This book offers the collaborative expertise of dozens of critical care physicians from different specialities, including but not limited to: emergency medicine, surgery, medicine and anaesthesia. Divided into sections by medical entities, it covers essential topics that are likely to be encountered in the emergency department where critical care often begins. The portable format and bullet point style content allows all practitioners instant access to the principle information that is necessary for the diagnosis and management of critical care patients.

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Contents


Page 3 of 3


  • 47 - Rhabdomyolysis
    pp 320-324
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of massive hemoptysis. Worldwide, tuberculosis (TB) is the most common cause of massive hemoptysis. In the United States, patients frequently have a history of pulmonary disease and/or smoking, cancer, prior hemoptysis, immunosuppression, cardiac disease, or coagulopathy/anticoagulant use. Patients may present with a sentinel bleed, with only a small amount of initial hemoptysis. The clinical course of these patients is difficult to predict, as small amounts of hemoptysis may suddenly become massive. Patients may present to the ED in extremis with active hemorrhage and respiratory failure. If the patient does not have active bleeding and is stable enough to go to radiology, chest CT may assist finding the etiology of hemoptysis. Bronchiectasis, lung abscess, pulmonary artery aneurysm, pulmonary embolism, and mass lesions are all abnormalities that can be identified by chest CT.
  • Section 8 - Hematology–oncology emergencies
    pp 325-356
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of pulmonary embolism (PE). The evaluation for suspected PE is tailored to the level of the clinician's suspicion for this diagnosis based on the patient's history, physical examination, and risk factors. A chest radiograph is rarely diagnostic for PE, but can identify alternative diagnoses. Hampton's hump, a pleural-based, wedge-shaped area of infiltrate, can be seen in pulmonary infarction and is suggestive of PE. Patients diagnosed with PE should be started on anticoagulation unless otherwise contraindicated to prevent clot propagation. Patients with a high clinical probability of PE should be started on anticoagulation therapy while awaiting diagnostic confirmation. The most common causes for sudden decompensation are respiratory and hemodynamic as the result of sudden shift or increase in clot burden. Intubation may be necessary to improve oxygenation/ventilation and establish control of the airway of the patient with PE.
  • 49 - Disseminated intravascular coagulation and thrombotic thrombocytopenic purpura/hemolytic uremic syndrome
    pp 330-336
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of gastrointestinal bleeding including upper gastrointestinal bleeding (UGIB) and lower gastrointestinal bleeding (LGIB). It describes the special circumstances with regard to aortoenteric fistula, liver disease, and Jehovah's Witnesses. In UGIB, patients typically present with hematemesis, coffee-ground emesis, and/or melena. In LGIB, patients typically present with bright red blood per rectum (BRBPR), also known as hematochezia. Higher severity of disease is indicated by signs of shock such as hypotension, tachycardia, altered mental status (AMS), decreased urine output (UOP), cool skin, syncope, orthostasis. Change in pulse with posture is more sensitive than hypotension, but may be masked by medications (e.g., beta-blockers). Hypotension, tachycardia, and tachypnea can indicate hemorrhagic shock and requires immediate treatment. Massive transfusion protocols are helpful for significant bleeding in order to prevent further coagulopathy due to transfusion of high volume of crystalloid or only red cells.
  • 51 - Tumor lysis syndrome
    pp 343-347
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of abdominal aortic aneurysms (AAA). The classic triad of ruptured AAA is hypotension, pain, and pulsatile abdominal mass. This occurs in only half of the patients. Typical pain is usually described as abdominal or lower back. Any patient with these symptoms and a known AAA is at risk for imminent rupture, if rupture has not already occurred. Vital sign stability should not be reassuring as these patients can deteriorate rapidly. Hypotension is the least consistent part of the triad, occurring in as few as one third of patients. Inflammatory aneurysms may present with fever or weight loss. Patients may complain of pain in the chest, thigh, inguinal area, or scrotum. Initial blood loss may be minor and the patient may present with normal vital signs. Vital sign stability should not necessarily be reassuring as these patients can deteriorate rapidly.
  • 52 - Sickle cell emergencies
    pp 348-356
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of acute pancreatitis. Historical features of pancreatitis include its characteristic abdominal pain, classically described as epigastric in location and radiating to the back. This is typically associated with nausea and vomiting. Multiple scoring systems have been developed to predict the severity of illness in acute pancreatitis, but none of them should replace regular reassessment of the patient's clinical condition. The most commonly used scoring system is the Ranson score. A frequently cited definition of pancreatitis is the presence of at least two of the following: upper abdominal pain; serum lipase at least 3 times greater than the upper limit of normal; and CT findings suggestive of acute pancreatitis. Laboratory findings in acute pancreatitis most importantly include elevated serum levels of lipase and amylase.
  • Section 9 - Infectious disease emergencies
    pp 357-388
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of fulminant hepatic failure. Patients can present with hypotension due to generalized systemic inflammatory response, coagulopathy, and encephalopathy with progression to coma and brain herniation. Diagnosis is based on clinical presentation and laboratory findings. Critical care management should be performed for cardiovascular, pulmonary, and infectious complications and other comorbidities. Prognosis and treatment decisions can be based on Rumack-Matthew nomogram. Renal failure occurs in up to 50% of cases, even more frequently in acetaminophen toxicity. In most cases continuous renal replacement therapy is indicated. Intermittent hemodialysis should be avoided as some evidence suggests rapid fluid shifts lead to brain herniation. Patients should be transferred to a transplantation facility as soon as possible. If a transplantation center is not readily available, consider transfer to a center that utilizes molecular adsorbents recirculation system (MARS) or artificial extracorporeal liver support therapy.
  • 54 - Pneumonia
    pp 362-366
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of acute mesenteric ischemia. The diagnosis should be considered in those older than 50 years, presenting with nonspecific abdominal pain and risk factors for the disease. The physician must have a high index of suspicion as the history of the disease may be difficult to obtain. The chapter lists clinical presentations of the subtypes of mesenteric ischemia. Emergent laparotomy is indicated, especially if signs of peritonitis are present. Surgery is generally the standard of care for mesenteric arterial embolism and thrombosis. Surgery is done to determine the extent of damage, to find the underlying cause, to revascularize viable bowel, and to resect infarcted bowel. Second-look procedures are often performed 24-48 hours after the initial surgery in order to restore continuity and assess extension of ischemia to ensure that at-risk or ischemic bowel is not used for the final anastomosis.
  • 55 - Meningitis and encephalitis
    pp 367-370
  • View abstract

    Summary

    This chapter discusses the management of surgical abdomen. It presents special circumstances, which make management of surgical abdomen difficult in some patients, including children, developmentally delayed, or obtunded individuals (from illness or drugs), patients with spinal cord injuries, pregnant patients, elderly or immunosuppressed patients, and morbid obese patients. Patients could present with referred pain, which is pain experienced at a site (or sites) distant from the initiating organ due to a shared neural origin with another body organ, such as right shoulder pain due to biliary colic or back pain due to pancreatitis. Acute-onset pain lasting longer than 6 hours in a previously healthy patient is often due to a surgical condition. As with the stable patient, a well-formulated differential diagnosis based on careful history and physical examination guides the plan of care far better than a shotgun approach of imaging and laboratory tests.
  • 56 - Infective endocarditis
    pp 371-374
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of abdominal compartment syndrome (ACS). The neurological presentation for the ACS includes increased intra-abdominal pressure (IAP) that is shown to decrease cerebral perfusion pressure by decreased cardiac output (CO) and hypotension, as well as via increased thoracic pressure with functional obstruction of cerebral venous outflow. The most efficient way to recognize and treat ACS is by recognizing and correcting predisposing factors before ACS occurs. In the closed abdomen, the gold standard approach to measure IAP uses a urinary bladder catheter (bladder pressures) with the patient in full supine position. Early recognition of risk factors and delaying definitive abdominal wall closure remains the best therapy for ACS. In cases in which the abdominal wall is already closed or the decompression is inadequate, timely intervention can be life-saving. ACS can occur even in the already decompressed abdomen.
  • 57 - Necrotizing soft tissue and skin infections
    pp 375-380
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of esophageal perforation and mediastinitis. About a third of patients present with atypical symptoms or signs including sepsis, peritonitis, respiratory distress, fever, pneumo/hydrothorax, fulminant shock, and multi-system organ failure. Approximately 17% of esophageal perforations are diagnosed only at autopsy. 90% of patients have findings suggestive of perforation on simple chest radiography. A contrast study such as esophagography with Gastrograffin should be performed if perforation is suspected. Although barium has superior sensitivity, it causes a worsened mediastinal/peritoneal inflammatory response if a leak is present. In addition, Gastrograffin is recommended because it does not obscure visualization during endoscopy. Computed tomography (CT) of the chest and abdomen with oral contrast may better define the leak, assess complications, and exclude other diagnoses.
  • 58 - Complications of human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS)
    pp 381-388
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of small bowel obstruction (SBO). It details the specific types of small bowel obstruction. Common causes of small bowel obstruction include hernias, neoplasms, intussusception, and others. Thorough history should be taken, with particular attention paid to prior SBOs, abdominal surgeries, hernias, cancer, and opiate use. The vital signs of SBO are: fever, tachycardia, hypotension, and tachypnea. The examination of the abdomen is performed by visually inspecting the abdomen for scars and distension. Rectal examination is considered with evaluation for occult blood, although diagnostic yield may below and classically the rectal vault will be empty. In laboratory evaluation findings are not specific to bowel obstruction. Results may show evidence of dehydration, acidosis, renal failure, and leukocytosis. Antibiotics are indicated with evidence of ischemia, perforation, or severe disease, although there is no good evidence supporting or refuting the use of empiric broad-spectrum antibiotics.
  • Section 10 - Endocrine emergencies
    pp 389-412
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of renal emergencies including metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis. The symptoms depend on the severity and etiology of the underlying acidosis, and are often nonspecific. Altered mental status, weakness, nausea, and abdominal pain are common. Hyperkalemia is often present due to transcellular shift of K-plus out of cells and H-plus into cells. Kussmaul respirations are classically associated with diabetic ketoacidosis (DKA), and refer to rapid, deep breathing. The critical presentation includes extreme acidemia that leads to neurological dysfunction (severe obtundation, coma, and seizures) as well as cardiovascular complications (arrhythmias, decreased cardiac contractility, arteriolar vasodilation, and decreased responsiveness to catecholamines). Profound hypotension and shock can result, which can complicate management since hypotension and shock are often the cause of the acidosis. If acidosis is due to DKA, treatment requires insulin and IV fluid resuscitation.
  • 61 - Adrenal crisis
    pp 403-407
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of common electrolyte disorders that include hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia, hypomagnesemia and hypermagnesemia. The signs and symptoms of moderate hyponatremia are non-specific such as generalized weakness, lethargy, nausea, vomiting, and muscle cramps. Hyponatremia is most commonly caused by an excess of antidiuretic hormone (ADH) released in response to intravascular volume depletion, exacerbated by volume replacement with hypotonic fluids. Overly rapid correction of hypernatremia may lead to cerebral edema and seizure. As with hyponatremia, to ensure a safe and accurate replacement rate, serum sodium levels have to be checked frequently. Release of calcium stores in the circulation is regulated by extracellular calcium concentration, parathyroid hormone (PTH), vitamin D metabolites, and calcitonin. Mild hypomagnesemia is usually asymptomatic, but failure to correct low serum magnesium may contribute to refractory hypokalemia and hypocalcemia.
  • 62 - Pheochromocytoma
    pp 408-412
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of acute kidney injury (AKI). It describes special circumstances for diagnosis and management of acute interstitial nephritis, contrast-induced nephropathy and rhabdomyolysis. A careful patient history frequently reveals etiology of renal failure (e.g., medications or recent administration of contrast dye). A careful patient history and appropriate laboratory testing should reveal the cause of AKI. Once AKI is diagnosed, all drugs that cause renal injury should be discontinued. Volume overload due to AKI can lead to pulmonary edema, which may require respiratory support including noninvasive positive-pressure ventilation or intubation. Patients with AKI who suddenly decompensate should be rapidly evaluated for electrolyte imbalances. Hyperkalemia, which can cause cardiac arrhythmias, is the most concerning. AKI resulting in metabolic acidosis can cause hypotension. Temporary treatment includes volume resuscitation and vasopressors. A sodium bicarbonate infusion can be considered while preparing for dialysis.
  • Section 11 - Environmental emergencies
    pp 413-450
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of rhabdomyolysis. Physical examination of a patient with rhabdomyolysis may reveal muscle swelling and tenderness, with occasional skin changes including discoloration, induration, and blistering. It is possible for rhabdomyolysis to present without any of these signs or symptoms, making serum markers essential to the diagnosis. Severe cases may present with hypovolemic shock, acute kidney injury (AKI), metabolic acidosis, disseminated intravascular coagulation (DIC), compartment syndrome, hyperkalemia, and cardiac arrhythmias. Compartment syndrome occurs due to swelling and edema of the injured muscle: classic physical examination findings include pain, paresthesias, paralysis, pallor, and pulselessness. The cornerstone of management includes discontinuation of inciting factors and aggressive management of fluid and electrolyte abnormalities. Intravenous fluids enhance renal perfusion and increase urinary flow in order to prevent AKI and increase potassium excretion.
  • 64 - Hyperthermia
    pp 418-426
  • View abstract

    Summary

    This chapter discusses the management of hematology-oncology emergencies including anticoagulation. Patients on anticoagulation who fall may have no immediate sequelae of an intracranial hemorrhage (ICH). Symptoms can develop over days or even weeks. The most common presentation of intracranial hemorrhage is an insidious onset of headache, light-headedness, nausea, and vomiting. Emergency physicians must maintain a high level of suspicion for intracranial bleeding in patients on anticoagulation, even in the absence of trauma, and particularly in those patients with a supratherapeutic INR. In anticoagulated patients with altered mental status or possible head trauma, a non-contrast computed tomography (CT) is key in identifying intracranial hemorrhage. Anticoagulated patients with head trauma, no loss of consciousness, and a negative initial head imaging should be observed for at least 6 hours (the exact number of hours is controversial) from the onset of the trauma.
  • 66 - Overdoses
    pp 431-450
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of disseminated intravascular coagulation and thrombotic thrombocytopenic purpura (TTP)/hemolytic uremic syndrome (HUS). The classic presentation of TTP involves a pentad of symptoms that include fever, neurological signs, anemia, thrombocytopenia, and renal dysfunction. This collection of symptoms is only seen in 20-30% of cases and it is strongly recommended to suspect the condition and manage it as such if a patient exhibits three or more of those features. HUS is most commonly seen in children and often follows an infectious illness, usually diarrhea. Morbidity and mortality in patients with TTP/HUS are usually attributed to thrombosis rather than anemia and bleeding. Patients with TTP can present with neurological symptoms that can be life threatening themselves or complicated by a life-threatening event. Patients (usually children) presenting with HUS may have significant renal dysfunction requiring dialysis.
  • Section 12 - End of life
    pp 451-456
  • View abstract

    Summary

    This chapter discusses the diagnosis, evaluation and management of neutropenic fever. The initial presentation of the critically ill with neutropenic fever may be overt with a clinical presentation similar to that of septic shock and including hypotension, respiratory failure, or any other major organ dysfunction. It may also be cryptogenic with isolated confusion, coagulopathy, or cardiac arrhythmias. Elderly patients and those taking steroids may present as hypothermic or euthermic. Any unexplained acute clinical deterioration should be considered a fever equivalent. Critically ill patients with neutropenic fever will most frequently present with common infections. However, their immunocompromised state places them at risk for more complex disease processes of almost any organ system. The pathophysiology of the decompensating patient with neutropenic fever is similar to that of a patient in septic shock. Those patients should be resuscitated similarly by the rapid and aggressive administration of crystalloids.

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