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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
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USMLE Step 2 CK
l Internal Medicine
The same is true of insect stings. Although bees may be common, patients can conceivably be
allergic to any insect’s venom.
Clinical Presentation. Mild symptoms include a rash known as “hives.” More severe symptoms include dyspnea, stridor, tachycardia, hypotension, and hemodynamic collapse.
Treatment. Mild allergies may respond to simply stopping the offending toxin and waiting.
More severe symptoms require the use of an antihistamine, such as diphenhydramine. Severe
symptoms of anaphylaxis with hemodynamic instability require epinephrine injections, IV fluids, antihistamines, and systemic corticosteroids.
VENOMOUS BITES AND STINGS
Cat and Dog Bites
Epidemiology. Dog bites are the most common bites in the United States.
Etiology/Presentation. Dog bites are usually ripping and tearing in nature, whereas, cat bites
are usually in the form of a puncture wound. Infection is more likely in patients with a delay
in treatment, extremes of age and extremity injuries. Infections are most often polymicrobial.
Cat bites are highly associated with Pasteurella multocida and dog bites are associated with
Pasteurella, Eikenella, hemolytic streptococci, Staph aureus, and Capnocytophaga canimorsus.
Note
All human and monkey
bites should always receive
prophylactic antibiotics.
Treatment. This includes exploration, debridement, irrigation, and proper wound care. If
prophylactic antibiotics are indicated, the drug of choice is amoxicillin and clavulanate (a
combination of clindamycin plus ciprofloxacin or trimethoprim/sulfamethoxazole or doxycycline can be used with penicillin allergy). Moxifloxacin may be used alone, as it has good
aerobic and anaerobic activity.
Indications for antibiotic prophylaxis:
• For any cat bite
• Any bite on hand, face, or genitals
• Immunocompromised patients
• Asplenic patients (high risk of overwhelming sepsis from Capnocytophaga canimorsus)
Most wounds should be left unsutured except for facial wounds for cosmetic reasons. Never
suture the hand.
Human Bites
Epidemiology. Human bites carry an infection rate of 15%, which is greater than cat and dog
bites together.
Etiology. The most common organisms are anaerobic and aerobic bacteria, specifically,
Eikenella corrodens. Hepatitis B and HIV can also be transmitted through bites but are much
less common.
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Treatment. Clean and irrigate wound well. No place for cultures on fresh bites. If the bite
is <12 hours old, close loosely. Give counseling for tetanus, hepatitis B, and prophylaxis.
Initiate 5 to 7 day course of prophylactic antibiotics.
Chapter 10
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Rabies
Epidemiology. Carried by raccoons, rats, wild dogs, woodchucks, skunks, foxes. Nearly 100%
fatal once the disease has been contracted. Bats are the most common cause.
Etiology/Clinical Presentation. Incubation period up to 1 year. Prodrome of 2 to 10 days
including fevers and paresthesias at the bite site. Neurologic changes include aphasia, paralysis, hypersalivation, and myoclonus.
Diagnosis. Viral cultures from saliva, CSF, or serum
Treatment. Ribavirin has been used in confirmed cases. Prophylaxis with human rabies
immunoglobin (HR16), which gives immediate passive immunity, and human diploid cell
vaccine (HDCV) should be given. The current guidelines for rabies vaccination are as follows:
• Preventive vaccination (no exposure) (usually 3 doses)
– Those at high risk of exposure to rabies (veterinarians, animal handlers, rabies lab
workers, etc.) should be offered the vaccine
– Those whose activities bring them into frequent contact with rabies virus or poten-
tially rabid animals (e.g., an international traveler who is likely to come into contact
with animals in a region where rabies is common) should be offered the vaccine
• Vaccination post-exposure
– Those who have been bitten by an animal or who may have been exposed to rabies
should receive wound cleaning and started on vaccine
º If had never been vaccinated against rabies: give 4 doses (1 dose right away and
additional doses on days 3, 7, and 14); a rabies immune globulin should also be
given at the first dose
º If had been previously vaccinated against rabies, give 2 doses (1 dose right away
and another on day 3); rabies immune globulin is not needed
l Emergency Medicine
Snakebites
Epidemiology. Although 50,000 snakebites are reported per year worldwide, only about 8,000
of those are poisonous. There are <5–10 deaths per year, with rattlesnakes accounting for
almost all fatalities.
Mechanism. Snake venom contains numerous potentially dangerous substances, such as
hemolysis toxin, cardiotoxin, neurotoxin, and proteolytic enzymes, in addition to others.
Some of these substances can result in neuromuscular blockade.
Factors that affect the severity of the bite:
• Body size. The smaller the body, the worse the effects; hence, bites tend to be worse in
children.
• Location of bite. Trunk and face bites are worse than extremity bites.
• Exercising after bite. Muscular activity helps spread the venom through the lymphatics.
• Depth of injury. No poisoning occurs in 20-50% of bites because they are too superficial.
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USMLE Step 2 CK
l Internal Medicine
Treatment. Transport the patient immediately to the nearest medical facility.
1. Immobilize the patient. This will help to decrease the spread of venom through the
lymphatics, which increases with muscular contraction.
2. Apply compression bandage. This will also help to decrease lymph flow. It should not
be so tight as to decrease venous flow.
3. Antivenin. Be cautious of anaphylactic reactions that may occur to the horse serum.
4. Supportive. Hypotension is managed with fluids. Ventilatory support may be necessary.
Ineffective therapy includes incision and suction of the bites. Tourniquets and ice immersion
do not help and might be harmful.
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Neurology
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Chapter Title
Learning Objectives
❏ Outline the presentation, diagnosis, and management of disease of the spinal cord
including spinal cord compression, syringomyelia, subacute combined degeneration,
anterior spinal artery occlusion, ALS, and Brown-Sequard syndrome
❏ Describe the epidemiology, classification, and treatment of seizures and epilepsy
❏ Describe the presentation, diagnosis, and management of movement disorders
including benign essential tremor, restless leg syndrome, Huntington disease, and
Parkinson disease
❏ Present the diagnosis and management of autoimmune neurological diseases,
including Guillain-Barre syndrome, MS, and myasthenia gravis
❏ Provide a differential diagnosis and work-up of patients presenting with headache,
vertigo, or dizziness
00
11
❏ List the criteria for prevention of cerebrovascular accident in patients with TIA, and
outline the management of patients with acute cerebrovascular accident
❏ Describe the epidemiology of dementia and typical course and complications
SPINAL CORD COMPRESSION
A 63-year-old African-American man is brought to the emergency department
complaining of back pain that started gradually 3 days ago. The patient describes
the pain as “band-like” around the abdomen, without radiation. His past medical
history is significant for prostate cancer, diagnosed 3 years earlier, and treated
with radiation.
Definition. An acute syndrome of back pain associated with compression of the spinal cord.
It is considered a neurologic emergency.
Etiology. Commonly caused by cancer (lymphoma; multiple myeloma; carcinomas of prostate, lung, breast, kidney, or colon), herniated disk, epidural abscess, hematoma, or trauma.
Acute cases are caused by trauma.
Note
Spinal Cord Compression
Acute: trauma
Subacute: most common
cause—neoplams
Chronic: herniation
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USMLE Step 2 CK
l Internal Medicine
Clinical Presentation. Patients commonly present with insidious onset of mild sensory
disturbance, lower extremity weakness, and/or sphincter or sexual dysfunction. Pain is the
earliest symptom in the majority of patients (96%). Pain may be intensified by actions that
increase intrathoracic and thus cerebral spinal fluid pressure. The diagnosis of acute spinal
cord compression has to be suspected on the basis of the history and neurologic exam. The
importance of having a high index of suspicion for the diagnosis is essential to instituting
appropriate therapy early in the course of the disease. A history of cancer, fever, and bowel or
bladder incontinence/retention are all points in the clinical history that strongly suggest the
possibility of acute spinal cord compression. On neurologic exam, a dermatomal sensory level
with bilateral lower extremity weakness, increased lower extremity muscle tone, and upper
motor neuron signs below the level of compression are all consistent with the diagnosis of
acute cord compression. The thoracic cord is the most common site of compression (70%)
because the spinal cord is narrowest at that point. Symptoms may progress quickly.
Diagnosis. Plain x-rays are abnormal in 84 to 94% of all cases. The diagnostic test of choice
is an MRI of the spine. When MRI of the spine is contraindicated, CT myelogram is the diagnostic test of choice.
Treatment. High-dose dexamethasone should be started immediately once the diagnosis is
suspected. After the specific etiology is delineated more clearly by MRI, specific therapy may
be initiated. For radiosensitive tumors, such as lymphoma or multiple myeloma, radiation
therapy should be started as soon as possible. Surgical decompression is the treatment of
choice for a herniated disk, epidural abscess, or hematoma. The prognosis depends mainly on
the functional status of the patient at the time of presentation. Up to 80% of patients who are
initially able to ambulate retain that ability after treatment. Only 5% of patients without antigravity leg strength are able to ambulate after treatment.
SYRINGOMYELIA
Syringomyelia is defined as cavitation of the spinal cord. It occurs as either communicating
(with the CSF pathways) or noncommunicating. Communicating syringomyelia is usually
associated with the congenital Arnold Chiari malformation, whereas the noncommunicating
syringomyelia is typically secondary to trauma or tumors of the spinal cord.
In the cervical vertebrae of both gray and white matter, there is typically sensory dissociation
with impaired pain and temperature and intact sensation to light touch. The loss of pain and
temperature occurs in a cape-like distribution across the neck and arms. There is sparing of
tactile sensation, position, and vibratory sense. Reflexes are lost.
As the lesion enlarges, there may be lower motor neuron manifestations at the level of the
lesion with upper motor neuron signs below the lesion. Cavitation most commonly occurs at
the level of the cervical cord. MRI is the most accurate diagnostic test. Treatment is surgical,
but often unsatisfactory.
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Note cavitation of spinal
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cord in shaded area
Figure 11-1. Syringomyelia
SUBACUTE COMBINED DEGENERATION
Subacute combined degeneration occurs with vitamin B12 deficiency. Patients will complain of
distal paresthesias and weakness of the extremities followed by spastic paresis and ataxia. On
exam there is a combined deficit of vibration and proprioception with pyramidal signs (plantar extension and hyperreflexia). Diagnosis is established by finding a low serum vitamin B12
and treatment is with vitamin B12 replacement.
Chapter 11
● Neurology
ANTERIOR SPINAL ARTERY OCCLUSION
Anterior spinal artery occlusion presents with acute onset of flaccid paralysis that evolves into
a spastic paresis over days to weeks. Additionally, there is loss of pain and temperature sensation with sparing of vibration and position sense as the posterior columns are supplied by the
posterior spinal artery. Everything (motor, sensory, autonomic) is lost below the level of the
infarction with the striking exception of retained vibration and position sense. Treatment is
supportive.
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USMLE Step 2 CK
● Internal Medicine
Posterior column
Figure 11-2. Anterior Spinal Artery Occlusion
Note dorsal
columns remain intact
BROWN-SÉQUARD SYNDROME
Hemisection of the cord results in a lesion of each of the 3 main neural systems: the principal
upper motoneuron pathway of the corticospinal tract, one or both dorsal columns, and the
spinothalamic tract. The hallmark of a lesion to these 3 long tracts is presentation with
2 ipsilateral signs and 1 contralateral sign.
• Lesion of the corticospinal tract results in an ipsilateral spastic paresis below the level
of the injury.
• Lesion to the fasciculus gracilis or cuneatus results in an ipsilateral loss of joint position sense, tactile discrimination, and vibratory sensations below the lesion.
• Lesion of the spinothalamic tract results in a contralateral loss of pain and temperature sensation starting 1 or 2 segments below the level of the lesion.
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At the level of the lesion, there will be an ipsilateral loss of all sensation, including touch
modalities as well as pain and temperature, and an ipsilateral flaccid paralysis in muscles supplied by the injured spinal cord segments.
Figure 11-3. Hemisection: Brown-Séquard Syndrome
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CEREBROVASCULAR ACCIDENT (CVA)
A 56-year-old woman is brought to the emergency department by her daughter
complaining of sudden onset of right upper extremity weakness that began while
she was watching television early this morning. The daughter became concerned
when her mother was unable to talk in response to questions. Neurologic
examination shows right upper extremity weakness with pronator drift and right
facial nerve palsy. When questioned, the patient seems to understand what is
being said but cannot clearly respond.
Chapter 11
● Neurology
Definition. A sudden onset of a focal neurologic deficit.
Etiology. The principal mechanisms by which strokes occur are:
1. Large artery thrombosis
2. Small artery thrombosis (lacunar)
3. Embolic (cardiogenic or artery-to-artery)
4. Vascular dissection
5. Systemic hypertension
6. Bleeding
Clinical Presentation. Stroke should be considered in any patient who presents with acute
onset of a focal neurologic deficit. The specific clinical syndrome is determined by the mechanism and vascular territory affected. The blood supply to the brain is divided into two major
systems: the carotid (anterior) circulation, and the vertebrobasilar (posterior) circulation. The
major blood vessels comprising the anterior circulation include the anterior cerebral artery
(ACA) and middle cerebral artery (MCA).
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USMLE Step 2 CK
l Internal Medicine
Occlusion of the ACA presents with contralateral weakness and sensory loss in the leg more than
in the upper extremity. Urinary incontinence, confusion, and behavioral disturbances are common. Lower extremity weakness exceeds upper extremity weakness.
aic.cuhk.edu.hk/web8
Figure 11-4. CT Scan Demonstrating a Right MCA Infarction
Occlusion of the MCA presents with contralateral hemiplegia, hemisensory loss, and homonymous hemianopia with eyes deviated toward the cortical lesion. Dominant hemisphere
involvement results in aphasia. Nondominant hemisphere involvement results in preserved
speech, comprehension with confusion, and apraxia with spatial and constructional deficits.
The posterior circulation provides blood supply to the cerebellum, brain stem, occipital lobe
of the cortex, and pons. The major blood vessels that comprise the posterior circulation are
the posterior cerebral artery (PCA), basilar artery (BA), and vertebral arteries.
Table 11-1. Posterior Circulation Syndromes
Ipsilateral Contralateral
Web e r CN III Hemiplegia
Benedikt CN III Ataxia
Wallenberg Facial sensory loss Body sensory loss
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Occlusion of the PCA presents with contralateral homonymous hemianopia, visual halluci-
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nations, and agnosias. Occlusion of the penetrating branches of this vessel can result in CN
III palsy with contralateral hemiplegia (Weber syndrome) or CN III palsy with contralateral
ataxia or athetosis (Benedikt syndrome).
Specific syndromes associated with occlusion of basilar artery branches include the “lockedin syndrome” (paramedian branches), presenting as quadriparesis with intact vertical eye
movements; and Wallenberg syndrome (posterior inferior cerebellar artery), which presents
as ipsilateral facial sensory loss, contralateral body sensory loss, vertigo, ataxia, dysarthria, dysphagia, and Horner syndrome.
Occlusion of the major cerebellar arteries produces vertigo, vomiting, nystagmus, and ipsilateral limb ataxia.
Diagnosis. The initial test of choice will always be a noncontrast CT scan of the head. This
test is done to distinguish between hemorrhagic and ischemic stroke. Noncontrast CT is the
most sensitive test for detecting blood in the brain. CT scans are often negative for ischemia
within the first 48 hours after symptom onset. Diffusion-weighted MRI is the most accurate
test for detecting cerebral ischemia.
The diagnostic workup of patients with acute ischemic stroke involves searching for embolic
sources (echocardiogram, carotid duplex, and 24-hour Holter monitor). Also consider a workup
for inherited hypercoagulability. Subarachnoid hemorrhage is associated with EKG abnormalities such as ischemia or inverted T-waves, called cerebral T-waves. A “bubble study” is done on
the echocardiogram to detect the presence of a patent foramen ovale or other cardiac defect.
Chapter 11
l Neurology
Treatment. Tissue plasminogen activator is given if the patient presents within 3 hours of symptom onset. Contraindications to the use of tissue plasminogen activator include stroke or serious head trauma within 3 months, hemorrhage (GI or genitourinary) within 21 days, surgery
within 14 days, history of intracranial hemorrhage, BP >185/110 mm Hg, current use of anticoagulants, platelets <100,000/mm3, or coagulopathy (PT >15 seconds). Patients who receive tissue plasminogen activator in an appropriate manner have better neurologic function 3 months
after CVA as compared with patients who did not receive tissue plasminogen activator.
There is no clear benefit to the use of heparin with stroke. This is because of the increased risk
of bleeding. Any benefit is offset by adverse events associated with treatment. For every stroke
prevented, one intracranial hemorrhage is caused. Therefore, treatment with heparin in acute
ischemic stroke is always wrong.
Antiplatelet therapy is most useful in secondary prevention of ischemic stroke. Aspirin is considered first-line treatment for secondary prevention of ischemic stroke. Aspirin is started 24
hours after TPA. When patients have a known allergy to aspirin or continue to have recurrent
cerebrovascular events on aspirin alone, dipyridamole may be added or the patient may be
switched to clopidogrel to enhance antiplatelet therapy. Ticlopidine is no longer used because
the rates of thrombotic thrombocytopenic purpura and leukopenia are unacceptably high.
For those with a recurrent stroke while on aspirin, the single best answer is to add dipyridamole or switch to clopidogrel. Do not combine aspirin and clopidogrel for a stroke. Combination
of anti-platelet agents is used on coronary disease but not cerebral disease.
Subarachnoid hemorrhage is treated with nimodipine to reduce the risk of ischemic stroke.
Early surgical intervention to clip off the aneurysm or embolize the vessel with a catheter
should be done in good operative candidates. “Early” means within several days. Don’t wait
for the unrepaired aneurysm to rebleed. Unruptured aneurysms found incidentally should be
repaired if they exceed 10 mm in size.
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