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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
.pdf
USMLE Step 2 CK
l Internal Medicine
Alcoholic hallucinosis:
• May be confused with DT
• Starts 12–24 hours after last drink but can last days to weeks
• Paranoid psychosis without tremors and confusion
• Normal vital signs (no hypertension or tachycardia)
• No agitation
• Normal appearance except for auditory (most common), visual, or tactile
hallucinations
Wernicke encephalopathy:
• Confusion, ataxia, and ophthalmoplegia (nystagmus)
Korsakoff psychosis:
• Amnesia and confabulations
Treatment. Alcohol withdrawal has a very high mortality rate (5%).
Benzodiazepines can be life-saving (important to taper dose slowly). Diazepam and chlordiazepoxide are common, due to their long half-life. There is no role for anticonvulsants.
Antipsychotics such as haloperidol should be avoided because they can lower the seizure
threshold and cause prolonged QT interval.
Hydrate with isotonic fluids and electrolyte replacement.
Symptom-triggered therapy is recommended. A work-up for alternative diagnosis is also very
important.
• Use only lorazepam or oxazepam for cirrhosis
• CT head to look for intracranial bleed
• Lumbar puncture to rule out meningitis if there is a fever
• Chest x-ray: look for aspiration pneumonia
• High doses of thiamine IV for Wernicke and Korsakoff. Treatment for alchoholic hallucinosis is benzodiazipines and haldoperidol (there is no risk of siezures, so it can be
used here)
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HEAD TRAUMA
A 20-year-old man is playing football when he is struck in the head and loses
consciousness for a few minutes. He awakens and has some motor weakness of
his left arm, which seems to slowly worsen over the course of the next hour as
he is brought to the emergency department.
Definition. Any degree of traumatic brain injury resulting in a range of injury from scalp
laceration to headache to loss of consciousness or focal neurologic deficits. The term does not
imply a specific mechanism of injury. The injury can result in concussion, contusion, epidural
hematoma, subdural hematoma, or traumatic subarachnoid hemorrhage. Cerebral contusion
can progress to intraparenchymal hemorrhage.
Clinical Presentation. The presentation is often only suggestive of the degree of injury. The
specific injury can only be determined by the use of CT scanning. All forms of head trauma
can result in headache, amnesia, and loss of consciousness. The degree of amnesia is loosely
associated with the degree of head trauma. That is to say, the worse the trauma, the more
memory one loses. Memory loss starts from the time of the episode of injury and stretches
both forward (anterograde), in which one doesn’t remember events since the time of the
injury, as well as backward (retrograde), in which one forgets past events. Retrograde amnesia
starts from the time of the injury and moves further back in time depending on the severity of the injury. The more severe the injury, the further back in time you forget. Retrograde
amnesia is more common. Recovery of memory starts with recollection of the most distant
progressing to the most recent memories.
l Emergency Medicine
Loss of consciousness, although possible in any form of head trauma, is not always present,
even with relatively severe forms of brain injury. You can have very severe intracranial bleeding (such as a subdural hematoma) without a loss of consciousness. This is particularly true
of chronic subdural hematoma.
Concussion is generally not associated with focal neurologic findings, such as motor or sensory
deficits. The presence of focal findings, starting in order of highest frequency, is most commonly
associated with epidural and subdural hematomas and contusion.
Diagnosis. CT scanning of the head is the mainstay of diagnosis of brain injury. Contrast
enhancement is not necessary because blood does not enhance with contrast. Hemorrhage
should be visible instantly if present at the time of the initial presentation. When evaluating
head CT scans, subdural hematomas are crescent-shaped and epidural hematomas are lensshaped. Follow-up scanning is also accomplished with CT scanning when necessary. Skull
x-rays are always the wrong answer when presented as one of the diagnostic choices. Normal
x-rays do not exclude hemorrhage, and abnormal x-rays do not confirm the presence of a
hemorrhage. Cervical spine x-rays should be obtained in head trauma if there are focal findings consistent with a cervical radiculopathy or if spinal tenderness is present. Even without
these findings, you should have a very low threshold for obtaining cervical spine x-rays.
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wyomingbrain.com
(venous in origin; may be acute or chronic
and may or may not result in midline shift)
Figure 10-16.
(usually arterial and associated
with skull fractures)
Figure 10-18.
(petechial hemorrhage and/or edema,
which may worsen over days)
Note
A concussion is diagnosed
by a history of loss of
consciousness plus a negative
CT scan of the head.
l Internal Medicine
wyomingbrain.com
Figure 10-15. Subdural Hematoma
wyomingbrain.com
Epidural Hematoma
wyomingbrain.com
Cerebral Contusion
Figure 10-17. Depressed Skull Fracture
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Dr. Conrad Fischer
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Figure 10-19. CT Scan Demonstrating Subdural Hematoma with a Midline Shift
Chapter 10
l Emergency Medicine
Treatment. Severe intracranial hemorrhage should be managed by lowering the intracranial
pressure. This is accomplished acutely with hyperventilation to PCO2 of 30–35, which will cause
vasoconstriction of cerebral vessels, leading to a decrease in intracranial pressure. It should be
used in moderation and for limited amount of time.
Osmotic diuretics such as mannitol and elevation of the head of the bed are also helpful to
reduce intracranial pressure. This is in preparation for surgical evacuation. Steroids are not
effective, and when an answer choice in head trauma is a steroid, it is always wrong. Select simpler measures such as elevation of the head of the bed to 30 degrees and maintenance of systolic
blood pressure to 110–160 mm Hg. This slight degree of hypertension assures that the cerebral
perfusion pressure is adequate.
Cerebral perfusion pressure is best when mean arterial pressure ≥60 mm Hg above the intracranial pressure. Stress ulcer prophylaxis with PPI is used after all severe head trauma and after
intubation.
SUBARACHNOID HEMORRHAGE
A 52-year-old woman is at her job in the office when she develops the sudden
onset of a severe headache, stiff neck, photophobia, and loss of consciousness. She
awakens within the hour that she arrived in the hospital. She is noted to have a
severe headache, nuchal rigidity, photophobia, and a temperature of 38.5 C (101.3 F).
Definition. A subarachnoid hemorrhage (SAH) is the sudden onset of bleeding into the subarachnoid space.
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l Internal Medicine
Etiology. Aneurysm formation is the most common etiology. The aneurysms can be saccular
or fusiform and are most commonly around the circle of Willis. The most common sites are
anterior communicating artery, middle cerebral artery, and posterior communicating artery.
There is an association with polycystic kidney disease, Ehlers-Danlos syndrome, and some
other connective tissue diseases. SAH most commonly occurs spontaneously. Head trauma is
rare as a cause of SAH.
Clinical Presentation. Sudden onset of severe headache is the hallmark of SAH. The sudden
rise in intracranial pressure results in loss of consciousness in as many as 50% of patients.
Focal neurologic symptoms occur in >30%, the most common from compression of the occulomotor cranial nerve. Sometimes the pressure of the bleed can dissect into the surrounding
tissues and cause other neurologic defects. Nuchal rigidity, photophobia, headache, and papilledema occur because of meningeal irritation. Fever can occur 3–4 days after the initial hemorrhage. This can simulate meningitis because an SAH is a form of chemical meningitis from
irritation by the blood. Seizures are also an extremely common finding. One-year mortality can
be up to 50%, with half of the people dying upon immediate occurrence of the bleed.
Note
A spinal headache may occur
after a lumbar puncture in
some patients. This is treated
with a blood patch.
Clinical Pearl
Traumatic lumbar puncture
may cause RBC in the CSF,
but xanthochromia is absent.
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Figure 10-20. Subarachnoid Hemorrhage on CT Scan
Longer-term manifestations include the development of focal deficits, seizures, rebleeding, and
hydrocephalus. Vasospasm after the bleed results in hypoperfusion to portions of the brain
parenchyma and the development of stroke. Rebleeding occurs when the clot falls off of the
original site of bleeding. Up to half of the people who rebleed will die. Hydrocephalus occurs
when the blood cells clog up the arachnoid granulations through which CSF normally drains.
Diagnosis. The initial test is the CT scan, which is more sensitive than MRI for the diagnosis
of SAH. The CT scan of the head is without the use of contrast and has a sensitivity of 90–95%
within the first 24 hours after the onset of the bleed. The diagnostic sensitivity of the CT scan
actually diminishes with time as the red cells within the CSF hemolyze and are resorbed and
converted into the yellowish coloring described on CSF examination as xanthochromia.
Chapter 10
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If the initial CT scan is normal and an SAH is still suspected, a lumbar puncture is done. The
lumbar puncture is the most sensitive diagnostic test. The absence of red cells and xanthochromia on the lumbar puncture essentially excludes an SAH. Xanthochromia is due to lysis
of RBCs and formation of bilirubin (straw-colored CSF). Xanthochromia needs 4–6 hours
to develop. Angiography is used to determine the specific anatomic site of the vascular defect
and the site of the bleeding. EKG abnormalities, such as inverted or enlarged T-waves, are
often associated with the development of an SAH and are not a cause for alarm.
Treatment. Initially, management consists of maintaining systolic blood pressure at 110-160
mm Hg. Pressure higher than this can provoke more bleeding. Pressure lower than this can
provoke cerebral ischemia through hypoperfusion, given the increased intracranial pressure.
Seizure prophylaxis is not necessary in these patients.
Corticosteroids are used to prevent hydrocephalus. Nimodipine is a calcium-channel antagonist that can be used to lower the risk of spasm in the blood vessel and therefore, lower the
risk of subsequent stroke. Angiography should be done to determine the anatomic site that
will need catheter or surgical correction. It is important to perform this so that surgical correction (usually performed through embolization or clipping of the AVM) can occur before
rebleeding develops. If hydrocephalus occurs, then shunting will be needed. Embolization is
superior to surgical clipping.
l Emergency Medicine
BURNS
A 32-year-old fireman is caught in a fire and is briefly trapped under a burning
staircase. He is quickly extracted and brought to the emergency department. His
respiratory rate is 14/min. He is fully alert and weighs 220 pounds. There is soot
in his mouth and nose and on his face, and his sputum not carbonaceous. The
nasal hairs are singed. He has no stridor or hoarseness, and the lungs are clear
to auscultation. He has first-degree burns on his right leg and second- and thirddegree burns on his right arm and chest.
Injuries due to burns can be divided into several types. The most common causes of death
from fires are smoke inhalation and carbon monoxide poisoning. Thermal injury is most
dangerous when it is respiratory related. Skin injury is labeled first degree when the skin is
fully intact, even though it may be discolored. First-degree burns are not associated with
blister formation and appear “sunburn-like.” The skin may be red or gray, but capillary refill
remains normal. Second-degree burns result in blister formation. Third-degree burns are
deeper and destroy skin appendages such as sweat glands, hair follicles, and sometimes pain
receptors. This leaves third-degree burns insensate. Pain perceived by third-degree-burn
patients is from surrounding structures where pain receptors are intact.
Pathophysiology. Although not apparent at first, respiratory injury can be the most lifethreatening injury. Soot in the mouth or nose, stridor, wheezing, altered mental status, burned
nasal hairs, and burns involving closed spaces are all clues to impending pulmonary and
laryngeal edema. Shock occurs not only from direct skin loss but also from the release of a
host of mediators that result in diffuse capillary leak for the first 18-24 hours. Serious capillary leak occurs when the percentage of serious body surface area burn exceeds 20-25%.
Note
Rule of Nines
The Rule of Nines differs
between adults and children.
Refer to Pediatrics for more
information on the treatment
and calculation of burns in
children.
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l Internal Medicine
Clinical Presentation. Altered mental status, dyspnea, headache, and chest pain are clues to
severe carbon monoxide poisoning. Laryngeal edema can result in stridor, hoarseness, and
dyspnea. Soot in the nose and mouth can imply impending airway compromise. Skin injury
is estimated with the “Rule of Nines” to assess fluid resuscitation. The head and arms are 9%
each. The chest, back, and legs are 18% each. Patchy burns can be estimated by using one
hand’s width as an estimate of 1% of body surface area burned. Circumferential burns are
critical in the assessment because as they heal they tighten and cut off circulation, leading to
limb compromise and the need for escharotomy.
Diagnosis. Besides the obvious burn, carboxyhemoglobin levels are essential in severe burns.
Severe burns are defined as combined second- and third-degree burns >20% in adults or >10%
in the very old or very young or third-degree burns >5% of body surface area (BSA). Chest
x-ray and bronchoscopy help determine the exact extent of respiratory injury when it is uncertain. Bronchoscopy can reveal severe thermal injury to the lungs even when the initial chest film
is normal. Foley catheter placement helps determine the adequacy of fluid resuscitation.
Treatment. If the patient has signs of severe respiratory injury, as described above, the first
step is to intubate the patient before more severe laryngeal edema can occur and make the
intubation difficult. If the carboxyhemoglobin level is significantly elevated (>5-10%), 100%
oxygen should be administered. Fluid resuscitation over the first 24 hours is based on a formula of 4 ml per % BSA burned per kg. Use Ringer’s lactate as the preferred fluid. Use second- and third- degree burns in your calculation. Give half the fluid in the first 8 hours, with
one-quarter in the second 8 hours, and one-quarter in the final 8 hours. This is known as the
Parkland formula. Afterward, when the diffuse capillary leak improves, give enough fluid to
maintain a urine output >0.5-1 mL per kg per hour.
Stress ulcer prophylaxis with H2 blockers or PPIs should be given. Topical treatment with
silver sulfadiazine is used to prevent infection. Do not break blisters and do not use steroids.
Escharotomy is useful in circumferential burns. Skin grafting is done on the basis of the size
and severity of the injury. Patients with burn injuries are at increased risk for pseudomonal
and staphylococcal infections; if there is concern for infection, give IV antibiotics that cover
these organisms.
Heat Disorders
Heat disorders are divided into 2 main groups: exertional and nonexertional. Exertional disorders vary from mild heat cramps to more severe heat exhaustion to potentially lethal heat stroke.
Nonexertional disorders are malignant hyperthermia and neuroleptic malignant syndrome.
• Heat Cramps. This is a mild disorder that can happen to any healthy person who
develops fluid and electrolyte depletion. The patient develops painful muscular contractions lasting a few minutes with muscle tenderness present. The patient is able to
sweat, and there are no neurologic abnormalities. The body temperature is normal.
Treatment is rest, oral rehydration, and salt replacement.
• Heat Exhaustion. This is a more severe exertional heat disorder. The patient is weaker
with more systemic symptoms. Body temperature may be slightly elevated. Mild neurologic symptoms such as headache, nausea, and anxiety may occur, but severe confusion is rare. Death is very unlikely, but the disorder can progress to heat stroke if not
treated. The patient is still able to sweat and remove heat from the body. Treatment
can be accomplished with oral fluid and electrolyte replacement, but with severe
weakness, the patient may need IV hydration.
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• Heat Stroke. This is a very severe and potentially life-threatening disorder. Most
patients have lost the ability to remove heat from the body because of the impairment
of the ability to sweat. Fifty percent of patients still retain some capacity to sweat,
but in insufficient amounts to keep up with heat generation. Body temperature may
become severely elevated (>41°C), resulting in confusion, disorientation, nausea,
blurred vision, and seizures. Numerous laboratory abnormalities may occur such as
hemoconcentration, rhabdomyolysis, and elevated BUN, creatinine, and white cell
count. Anuria, DIC, and lactic acidosis may develop.
• Treatment of heat stroke is with IV fluid replacement and rapid cooling of the body
(place in cool environment and spray with water, then fan to evaporate the fluid).
Ice-water immersion can result in overcooling and hypothermia. Chlorpromazine and
diazepam can be used to control shivering.
• Malignant Hyperthermia. This is a nonexertional heat disorder occurring as an idiosyncratic reaction to the use of anesthetic agents such as halothane or succinylcholine.
Virtually any anesthetic may cause it. Rhabdomyolysis may develop. Treatment is with
dantrolene.
• Neuroleptic Malignant Syndrome. This is an idiosyncratic reaction to a wide variety of phenothiazines or butyrophenones such as haloperidol. Muscular rigidity and
rhabdomyolysis may occur as well. Treatment, besides stopping the drug, is with bromocriptine or dantrolene.
l Emergency Medicine
Hypothermia
Definition. A reduction of core body temperature below 35°C (normal 37°C). Core temperature is measured with a rectal probe or through the esophagus. Severe hypothermia is a core
temperature below 30°C.
Etiology. Hypothermia often occurs in association with alcohol intoxication, particularly in
the elderly.
Clinical Presentation. The most common symptoms of severe hypothermia are related to the
central nervous system. Lethargy, confusion, and weakness may occur. Death is most commonly
from arrhythmia (Osborne wave or J wave). This is from the effect of the cold on altering cardiac conduction. Other complications include metabolic acidosis, respiratory acidosis, kidney
injury, and hyperkalemia.
Diagnosis. The EKG can show a wide variety of serious arrhythmias, including ventricular
fibrillation or ventricular tachycardia. The most characteristic finding is an elevation of the
J-point, known as Osborne waves. J-wave elevation may mimic ST-segment elevation.
Treatment. Most patients will respond well to common-sense treatment, such as a warm
bed, bath, or heated blankets. Warmed IV fluids or warmed humidified oxygen can be used
in very severe cases, although care must be taken because overly rapid rewarming can result
in arrhythmias as well. When life-threatening arrhythmias occur, it is important to continue
resuscitative efforts until the body temperature is >35°C. If the patient is cold but not shivering, active measures should be used:
Active external rewarming
•
Only to truncal areas
• Warm blankets
Note
Hypothermia must be worked
up for precipitant factors:
Hypoglycemia (most
•
common cause)
• Hypothyroidism
• Sepsis
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USMLE Step 2 CK
l Internal Medicine
• Heat lamps
• Hot-water bottles
Active internal rewarming
• Warm IVFs (45° C)
• Warm humidified oxygen (45° C)
• Warmed gastric lavage via NGT
• Warmed hemodialysis
Hypothermia is one of the few times in which a patient can be resuscitated from pulselessness
beyond the usual 10 minutes of efforts.
RADIATION INJURIES
Ionizing radiation damages tissues primarily through destructive changes to DNA molecules.
Ionizing radiation is lethal and can often cause cancer. Longer exposures give worse injury.
Nonionizing radiation is less destructive to tissue and causes injury primarily as burns.
Examples include infrared, ultraviolet, and microwave radiation.
Presentation. To give a sense of scale, mortality is almost zero with <2 Gy (or Sv) of exposure.
This rises almost to 100% mortality with >10 Gy (or Sv). (10 Gy = 1,000 rad.)
Any cell can be damaged by ionizing radiation, but the more rapidly the cell divides, the more
vulnerable it is to radiation. This is because more DNA damage can be done during the time
of division.
Bone Marrow. As little as 2-3 Gy (200-300 rad) can depress the lymphocyte count. Neutrophils
are the next most sensitive cell, and erythrocytes are the least sensitive. Long-term, leukemia is
the earliest and most common cause of cancer from radiation exposure. Thrombocytopenia can
result in death from bleeding. Overall, infection and bleeding from depressed bone marrow function are the most common causes of death in acute exposure.
Gonads. Two to 3 grays result in temporary aspermatogenesis. Four to 5 grays can make men
permanently sterile. Testes are more sensitive than ovaries.
GI. Nausea and vomiting are the most common early symptoms of radiation exposure. This
develops in 50% of cases with a 2 Gy (200 rad) exposure and in 100% of patients with >3 Gy
exposure. In addition to nausea and vomiting, the rapidly reproducing intestinal lining ulcerates, leading to bleeding and infection later.
Other Sites. Other common sites of radiation injury are the skin, salivary glands, respiratory
epithelium, and thyroid glands.
Treatment. The management of radiation injury is supportive only. There is no specific therapy to reverse radiation injury.
• Antiemetics. Given that nausea is such a common feature of radiation sickness, antiemetics are a mainstay of therapy.
• Blood products. Platelets and RBC transfusions are needed. WBC transfusions don’t help.
• Colony-stimulating factors (G-CSF, GM-CSF). These will help restore marrow function.
• Antibiotics. Use as needed when infection develops.
• Bone marrow transplantations. These are occasionally useful.
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l Emergency Medicine
DROWNING
Risk/Mechanism. Alcohol and drug use are strongly associated with an increased risk of death
by drowning. Muscular exhaustion, head and spinal trauma, or acute myocardial infarction
are also predispositions to drowning and near drowning. Ten to twenty percent of drowning
victims may have suffered dry drowning in that there is no water aspirated into the lungs. Dry
drowning is secondary to laryngospasm.
Drowning from aspiration of water can be divided into 2 types:
• Freshwater, which is hypotonic, alters pulmonary surfactant, resulting in unstable alveoli, which then collapse. The hypotonic freshwater is absorbed into the body, result-
ing in acute hypervolemia, hemodilution, and intravascular hemolysis. At autopsy,
the lungs may contain little water.
• With seawater, the hypertonic water draws water out of the body into the lung, causing
systemic hypovolemia and hemoconcentration. The lungs become even more heavy
and fluid-filled because the surfactant is essentially washed out.
Presentation. Only the presentation of near drowning is important to discuss because drowned
victims are dead. The presentation can vary from coma to agitation. Cyanosis, coughing, and
signs of pulmonary edema, such as tachypnea, tachycardia, and blood-tinged sputum, are common. Rales and rhonchi can be found on the exam. Hypothermia is also common.
Laboratory Findings. Arterial blood gases show hypoxia and hypercarbia, as well as metabolic acidosis from anaerobic metabolism. Hyperkalemia may be present if there is significant
hemolysis. Renal insufficiency on the basis of hypoxia is a rare finding.
Note
Near Drowning vs. Drowning
• Near drowning is survival
after immersion, at least
for some time. Morbidity is
high and death may occur
later. The exact definition
is still the topic of much
debate.
• Drowning is defined as
death within 24 hours after
submersion in water.
Treatment. The first task is to remove the patient from the water and do ABCs (airway/breathing/circulation) of resuscitation.
Endotracheal intubation as needed
•
• Supplemental oxygen
• Positive pressure mechanical ventilation as needed
After removal from water, establishment of adequate airway is the most important initial
step. Continuous positive airway pressure (CPAP) is the most effective treatment and gives
the best correction of hypoxia and acidosis. Even if the patient appears comfortable initially,
continue observation for 24 hours because ARDS (acute respiratory distress syndrome) may
develop as a late finding.
The following treatments do not help and may be harmful:
• Abdominal thrusts. These may lead to aspiration of gastric contents.
• Prophylactic antibiotics. Antibiotics are only indicated if pneumonia develops.
• Steroids. There are no benefits to administering steroids.
ANAPHYLAXIS
Definition. A syndrome of histaminergic release in which there are signs of severe injury such
as urticaria, angioedema, hypotension, tachycardia, and respiratory compromise.
Etiology. As an idiosyncratic reaction, patients can potentially develop anaphylaxis from any
food, medication, insect bite, or antigenic substance entering the body by oral or parenteral
route. Although medications such as penicillin, phenytoin, contrast agents, and allopurinol
are most often associated with anaphylaxis, patients can potentially be allergic to anything.
Chocolate, peanuts, and strawberries are common, but patients can be allergic to any food.
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