Read The Washington Manual Internship Survival Guide Online

Authors: Thomas M. de Fer,Eric Knoche,Gina Larossa,Heather Sateia

Tags: #Medical, #Internal Medicine

The Washington Manual Internship Survival Guide (23 page)

BOOK: The Washington Manual Internship Survival Guide
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  Typical signs and symptoms: Flaccid bullae and erosions with mucosal involvement (PV) and pruritus with tense bullae in an elderly person (BP).


  Workup and diagnosis: Skin biopsy with direct immunofluorescence (BP and PV) and serum for indirect immunofluorescence (PV).


  Treatment:

•  PV: Steroids, mycophenolate mofetil, azathioprine, rituximab.
•  BP: Steroids (topical or systemic), tetracycline, dapsone, nicotinamide, and mycophenolate mofetil.


  Clinical pearls: PV is associated with a higher mortality than BP. Thus, PV requires aggressive treatment. Most patients do not require hospitalization unless infected or having difficulty maintaining fluid balance. Etiologies of blistering diseases include infectious, autoimmune, allergic hypersensitivity, metabolic, paraneoplastic, and genetic.

Vasculitis


  Urgent consult.


  Pertinent info: Drug history, known connective tissue disease, malignancy, or infection.


  Typical skin findings:
palpable purpura
(dark reddish-purple lesions that do not blanch and may blister or ulcerate) on the lower extremities or dependent areas. Eruption may be itchy, painful, or asymptomatic.


  Workup: CBC, CMP, urinalysis, skin biopsy, CXR, throat culture for strep, ESR, hepatitis panel, cryoglobulins, ANA, RF, antiphospholipid antibody, ANCA, SPEP.


  Diagnosis: Skin biopsy; concern for systemic involvement if fever, arthralgias, abdominal pain, pulmonary symptoms, hematuria, or proteinuria.


  
Treatment:

•  
Discontinue potential causative drug
(e.g., ASA, sulfonamides, penicillin, barbiturates, amphetamines, PTU).
•  
Treat underlying disorder
(e.g., infection, malignancy, or connective tissue disease).
•  Antihistamines, NSAIDs, colchicine, dapsone, antimalarials.
•  If systemic involvement: Prednisone, azathioprine, cyclophosphamide, IVIG, plasmapheresis.


  Clinical pearls: Up to 50% of cases are idiopathic. Thrombocytopenia is associated with nonpalpable purpura. DIC and warfarin necrosis cause extensive purpura.
Neisseria
sepsis and Rocky Mountain spotted fever also cause petechiae and purpura. Acral hemorrhagic papules, pustules, or vesicles may result from thrombi or septic emboli.

Hypersensitivity Syndrome (Severe Drug Reaction)


  Urgent consult.


  Pertinent information: Drug history (sulfonamides, anticonvulsants, allopurinol).


  Physical exam: blanchable erythematous macules, exfoliative dermatitis, or EM (target-like) lesions; edema of face or extremities, fever, lymphadenopathy, hepatosplenomegaly.


  Workup: CBC (with eosinophil count), liver function panel, urinalysis, and CXR.


  Treatment:

•  
Stop offending drug.
•  Oral/topical steroids and antihistamines for symptoms.


  Clinical pearls: The syndrome, also known as
DRESS (“drug reaction with eosinophilia and systemic symptoms”)
, develops within 8 weeks of starting the causative drug. Up to 50% develop fulminant hepatic necrosis if the drug is not stopped early in the course. Some anticonvulsants cross-react in 70% to 80% of patients (phenytoin, carbamazepine, and phenobarbital). Valproic acid does not cross-react. Patients should warn first-degree relatives that they, too, may be at high risk for a reaction due to a hereditary component.

Erythroderma (Generalized Exfoliative Dermatitis)


  Urgent consult.


  Pertinent info: Prior skin disorder, drug history, duration of erythroderma.


  Physical exam: Diffuse erythema of skin leading to exfoliative dermatitis, pruritus, keratoderma, shivering/chills, alopecia.


  Most common causes: Idiopathic, drug reaction, lymphoma and leukemia (including cutaneous T-cell lymphoma), atopic dermatitis (eczema), psoriasis, contact dermatitis, seborrheic dermatitis.


  Labs: CBC, BMP, albumin, calcium, SPEP, peripheral blood smear for Sézary cells.


  Diagnosis: Clinical features, skin biopsy.


  Treatment:

•  Treat underlying skin condition if known (e.g., psoriasis, eczema).
•  Discontinue any suspect drugs.
•  Search for and treat underlying malignancy.
•  Topical steroid ointment (mid-potency, e.g., triamcinolone 0.1% ointment, consider wearing a sauna suit), emollients, systemic antihistamines.
•  Monitor closely for electrolyte and fluid imbalances, highoutput cardiac failure, renal failure, sepsis, and hypothermia.


  Clinical pearls: 20% of cases are idiopathic. The course and prognosis depend on the underlying etiology. A diligent search for the underlying cause is often required. Most patients do not require hospitalization unless infected.

NEUROLOGY

Acute Focal Neurologic Deficit (Stroke)


  
Emergent.
If the time of onset is known to be
within 4.5 hours, call neurology immediately, as the patient may be a candidate for thrombolytic therapy.


  Pertinent information: There are two broad categories of stroke:

•  
Ischemic
(including TIA): sudden-onset focal neurologic deficit attributable to a vascular territory. TIA is a focal deficit that completely resolves within 24 hours. Most clear within 5 to 10 minutes. Ischemic stroke accounts for more than 80% of strokes.
•  
Hemorrhagic
: Includes intracerebral hemorrhage and subarachnoid hemorrhage.
•  Symptoms and signs: Stroke causes negative neurologic symptoms, such as weakness, loss of sensation, visual loss, and aphasia. Positive symptoms, such as pain, paresthesias, jerking
movements, and hallucinations, are rare and suggest seizure. Headache can occur and is more common with hemorrhagic stroke than ischemic stroke.


  History:

•  What was the time of onset? This is the time the patient was last seen or known to be normal, not when he or she was found with the deficits. If the patient awakens with deficits, consider the time he or she went to sleep as the time of onset.
•  How did the symptoms begin (suddenly or gradually)? How are they progressing (stable, worsening, or improving)?
•  Are there associated symptoms (severe headache, nausea, or vomiting may suggest hemorrhagic stroke)?
•  Are there any known contraindications for thrombolytics (see below)?
•  What is the patient’s past neurologic, medical, and surgical history?
•  What are the patient’s medications (especially anticoagulants)?


  Physical exam: Check vital signs (especially blood pressure and oxygen saturation). Look for evidence of recent head injury. Oral trauma suggests unwitnessed seizure. Do a cardiopulmonary exam to evaluate for arrhythmia and concurrent cardiac ischemia and to monitor for signs of aspiration. Perform a focused neurologic exam.


  Workup: Immediate evaluation consists of a stat noncontrast head CT to evaluate for hemorrhage, finger stick glucose, stat CBC, and stat coagulation panel. Also check ECG, CXR, urine drug screen, troponin, and chemistry panel.


  Treatment of ischemic stroke:

•  If the time of onset is well established to be within 3 hours, and there are no contraindications for thrombolysis, then
IV TPA
is the only approved specific treatment for ischemic stroke. Strong contraindications for TPA include blood pressure >185/110; blood sugar >400 or <50; seizure at onset; stroke in the last 3 months; history of intracranial hemorrhage; anticoagulant therapy and INR >1.7 or elevated PTT; platelets <100; recent major surgery within 14 days; head injury within 3 months; GI or GU bleeding within 21 days; arterial puncture at a noncompressible site within 10 days; rapid improvement of symptoms. If the time of onset is between 3 and 4.5 hours, there are additional contraindications. These include age >80; anticoagulant use (even with
normal PT/INR); history of a prior disabling stroke AND diabetes.
•  Blood pressure management: Generally stroke patients are allowed to be hypertensive to improve perfusion to the ischemic penumbra. If the mean arterial pressure exceeds 130 mm Hg, consider a dose of
IV labetalol
(if HR >80) or
hydralazine
(if HR <80). If they have received TPA, there are tighter blood pressure goals to reduce the risk of hemorrhagic conversion. Treatment of the blood pressure is dependent on the risk of end-organ damage (i.e., cardiac ischemia, acute renal failure).
•  Airway management: Intubation may be required if the stroke has compromised level of consciousness to the degree that the patient is unable to maintain an adequate airway. This is seen most often in brain stem strokes and strokes affecting a large territory.
•  Reimaging is required if the patient develops worsening of the neurologic examination. Head CT is sufficient to evaluate for likely causes, such as hemorrhage, midline shift, herniation, and hydrocephalus.

Seizure


  Level of urgency: urgent or emergent. If the patient experiences multiple seizures, or has not returned to baseline, then an emergent neurology consult is indicated. If the patient has returned to baseline after a single convulsion, neurologic evaluation should be obtained on an urgent basis.


  Description:

•  Status epilepticus is defined as multiple seizures without regaining full consciousness between the episodes, or a single seizure that lasts longer than 5 minutes.
•  Symptoms and signs of focal brain disease: Patients may describe an aura prior to the episode or have postictal focal weakness.


  Pertinent history:

•  Has the patient returned to baseline?
•  Has he or she had seizures before?
•  What did the seizure look like (description of onset, movements, head turning, eye position, loss of continence, oral trauma, ability to respond to questions)?
•  Are there any known metabolic derangements (e.g., hypoglycemia or hyperglycemia)? Any known drug or toxic exposure?
•  
Any signs of infection?
•  Any history of head trauma?


  Physical exam: Evaluate for signs of head injury, oral trauma, or meningismus. Determine level of consciousness and assess for deficits of cranial nerves or motor function.


  Workup: Seizures are usually a symptom of an underlying problem. Consider a structural lesion (neuroimaging), metabolic derangements (check finger stick glucose, chemistry panel, magnesium, calcium), or infection (check urinalysis and CXR).


  Treatment: Most important, remain calm!

•  
Single seizure
: If the seizure is ongoing, note the time. Check for level of consciousness, ability to follow commands. Look for forced eye deviation or nystagmus. Protect the patient’s airway, but do not insert objects into the mouth if he or she is convulsing. Turn the patient on his or her side and pad the bedrails. Provide oxygen by face mask, check vital signs, obtain finger stick blood sugar. Anticonvulsants are not needed acutely for a single seizure.
•  
Status epilepticus
: If the seizure has been continuous for 5 minutes, or if there have been multiple seizures without full return to baseline, then the patient is in status.
This should be considered a neurologic “code.”
Protect the airway, have an intubation kit available, obtain ABG, cardiac monitor, and pulse oximetry (many of these monitors will be difficult to interpret if there are ongoing convulsions). Ensure multiple working IVs are in place. Do a stat finger stick glucose and send CBC, chemistry, magnesium, urine and serum toxicology, alcohol level, urinalysis, and drug levels for any anticonvulsants the patient should be taking. Give
thiamine 100 mg IV
followed immediately by
50 mL of 50% glucose
. Do not wait for the results of the Accu-Chek as hyperglycemia is transient and far less damaging than prolonged hypoglycemia.
▪  
Lorazepam
in 2 mg boluses, up to 0.1 mg/kg (4 to 8 mg) at a rate of 1 mg/min, should be administered IV if possible. PR diazepam (0.5 mg/kg to a maximum of 20 mg) or IM midazolam (0.2 mg/kg) can be given if there is no IV access. This should be repeated if there continues to be seizure activity.
▪  An intravenous anticonvulsant should rapidly follow the benzodiazepine, usually
phenytoin
(15 to 20 mg/kg). Blood pressure will need to be monitored, as this may cause hypotension. The maximal infusion rate is 50 mg/min.
Alternatively,
fosphenytoin
can be used. It can be infused at rates up to 150 mg/min and has less risk of hypotension and arrhythmia, but is a pro-drug that must be converted prior to becoming an active anticonvulsant.
•  If the patient continues to have refractory seizures, efforts should be made to transfer him or her to an ICU, with EEG monitoring. Aggressive anticonvulsant therapy requiring intubation and mechanical ventilation may be necessary.
BOOK: The Washington Manual Internship Survival Guide
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