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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Case 11
Chief Complaint
“I’ve had shortness of breath for 5 hours.”
History and Physical Examination
A 25-year-old man with no significant past medical history comes to the emergency
department with shortness of breath for the past 5 hours. He was reportedly doing well
until this afternoon when he had difficulty going up a flight of stairs after getting home
from the gym. He has never experienced this in the past. He reports having mild chest
pain, especially when taking a deep breath. He denies fever/chills, cough, recent travel,
and sick contacts. Additionally, he denies using tobacco products, and believes there is no
family history of hypercoaguability.
His temperature is T 37.2 C (99.0 F), blood pressure 118/65 mm Hg, pulse 105/min, and
respirations 24/min. Height is 6 ft (1.8 m) and weight 179 lbs (81 kg). He appears to be in
mild distress. Examination of the head and neck shows no abnormalities. No carotid bruits
are noted and the thyroid is not enlarged. Cardiac examination shows tachycardia without
murmurs, gallops, or rubs. The PMI is not displaced. Lung examination shows few
bibasilar rales. Abdominal examination is unremarkable. The extremities show no
cyanosis, clubbing, or edema. There is no calf tenderness or palpable cords.
Differential Diagnosis
Pneumothorax1.
291
Initial Management
Setting: emergency department or office
Diagnostic/Therapeutic Plan
CCS NOTE
Most of these tests will be completed simultaneously. While the results of the basic
chemistry panel, lactate, troponin, and proBNP are pending, the chest x-ray, EKG, and
ABG are being done. Results of these tests will be delivered within a short timeframe.
Pulmonary embolism (PE)
2.
Pneumonia
3.
Arrhythmia
4.
Acute coronary syndrome
5.
Pulse oximeter
Chest x-ray
EKG
ProBNP
Serum troponin
Lactate
ABG
Serum electrolytes, BUN, creatinine, glucose
D-dimer
PT/PTT/INR
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Test Results
Assessment
At this point, the patient is hypoxic, tachycardic, and has an elevated A-a gradient. The patient
is hemodynamically stable so the next step is CT angiogram of the chest (“gold standard”). A
V/Q scan can also be completed if the patient has renal failure or allergy to contrast dye.
Further Management Plan/Results
Treatment Plan
Pulse oximeter: 91% room air
Chest x-ray: bilateral atelectasis and bilateral small pleural effusions, no pneumothorax
seen
EKG: sinus tachycardia at 105/min, no ST/T wave changes
ProBNP: 800 pg/mL
Serum troponin: <0.01 ng/L
Lactate: 1.3 mg/dL
ABG: pH 7.46, PaO2 85 mm Hg, PaCO
2
30, HCO
3
25, oxygen saturation 92%
Serum electrolytes, BUN, creatinine, glucose: sodium 136 mEq/L, potassium 3.8 mEq/L,
chloride 103 mEq/L, bicarb 23 mEq/L, BUN 10, creatinine 0.7, glucose 89 mg/dL
D-dimer: 2000 mg/L
PT/PTT/INR: normal
Supplemental oxygen1.
CT angiogram: right-sided PE2.
Echocardiogram: normal RV size, no tricuspid regurgitation, EF 55–60%3.
Admit patient to telemetry floor4.
293
Since it has been determined that the patient has a PE, start anticoagulation therapy with IV
unfractionated heparin (UFH), fondaparinux, or low-molecular weight heparin (LMWH), with
the goal of simultaneous warfarin administration. LMWH has largely replaced UFH in the
treatment of acute VTE because it has more reliable pharmacokinetics and facilitates outpatient
management.
Warfarin therapy may be initiated on day 1 or 2 of heparin therapy. Because factor II and X
levels require at least 5 days to decline, parenteral anticoagulation should overlap with
warfarin for at least 5 days and until an INR ≥2 is achieved.
Rivaroxaban is approved by the FDA for the long-term prevention of recurrent PE; however,
due to the paucity of long-term experience with it, warfarin or LMWH is preferred.
In patients with advanced cancer, the duration of therapy is indefinite or as long the cancer is
active or being treated.
Placement of a vena cava filter is the appropriate treatment of acute deep venous thrombosis or
PE only in cases with contraindications to anticoagulation.
Persistent hypotension or shock (i.e., systolic BP <90 mm Hg or a decrease in systolic BP by
≥40 mm Hg from baseline) due to acute PE is the only widely accepted indication for
thrombolysis. Systemic thrombolytic therapy with tPA should be considered only after acute PE
has been confirmed because its adverse effects can be severe.
Additional workup for this young man with acute PE is warranted: lower extremity U/S
Doppler, genetic testing for a hypercoaguable state, and occult malignancy.
Follow-up Management
Currently, there are no guidelines for hypercoagulable workup for thromboembolic disease.
However, it is very important to consider age-appropriate malignancy workup. In the elderly,
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for example, a full malignancy workup (mammogram, colonoscopy, CT chest, abdomen and
pelvis, etc.) should be done. In this patient, a testicular exam would be appropriate.
Antiphospholipid antibodies should be considered because the antiphospholipid syndrome
should be anticoagulated for life. These patients are at risk for both arterial and venous
thromboemboli. They are also at increased risk for MI and cardiovascular mortality.
In women, it is important to test for factor V Leiden. Patients with factor V Leiden must not take
oral contraceptive pills because the risk of VTE is very high with this combination. Those
patients must also be anticoagulated with LMWH during pregnancy.
Lower extremity Doppler should be done to find the source. Most PEs originate as lower
extremity DVTs.
Discussion
The patient is presenting with acute PE. Patients with idiopathic (unprovoked) VTE are at high
risk for recurrence, with approximately 50% experiencing a recurrence within 10 years.
Guidelines recommend the following:
CLINICAL PEARL
Patients with a first episode of acute unprovoked PE (i.e., acute PE that is NOT due to a
temporary or reversible risk factor) should receive anticoagulant therapy for 6 months and
possibly longer.
Patients with recurrent acute PE should receive anticoagulant therapy indefinitely if they
have a low or intermediate risk of bleeding.
295
OPC and pregnancy can lead to a hypercoagulable state because estrogen causes an
increase in liver production of clotting factors.
Final Diagnosis
Pulmonary embolism
Basic Science Correlate
The 3 pathways which make up the classical blood coagulation pathway are as
follows:
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Source: Wikimedia
Thrombus Formation
Thrombi can appear grossly (and microscopically) as laminations called lines of Zahn; these
represent pale platelet and fibrin layers alternating with darker red cell–rich layers. Such lines
are significant in that they are only found in thrombi that form in flowing blood; their presence
can usually distinguish antemortem thrombosis from the bland nonlaminated clots that form in
the postmortem state. Factors which play a role in thrombus formation are:
Stasis or turbulent flow: immobility (e.g., surgery), aneurysm, atrial fibrillation,
cardiomyopathy
Endothelial damage
297
CLINICAL PEARL
Warfarin necrosis
Vitamin K dependent factors are VII, II, IX, X, protein C, and protein S. Warfarin
necrosis occurs in patients with protein C or S deficiency. When given warfarin,
protein C and S levels decrease before the other factors because they have a shorter
half-life and that leads to clot formation and necrosis of the fingers and toes. Prevent
this by anticoagulation with heparin first.
Hypercoagulable states
Common states: factor V Leiden (a mutation of factor V, which makes it unable to be
cleaved and inactivated), prothrombin mutation (G20210A variant); increased levels of
factor VII, IX, XI or fibrinogen
—
Rare states: antithrombin III deficiency, protein C and protein S deficiencies
—
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6
Hematology
Case 1
Chief Complaint
Fatigue, jaundice, back pain, dark urine, fever
History and Physical Examination
A 30-year-old man of Greek origin presents to the emergency department with complaints
of acute onset fatigue, back pain, and lightheadedness. He also notes the onset of jaundice
and dark urine over the past several hours. He recently ate in a Middle Eastern restaurant
but has no nausea or vomiting. He denies any bright-red blood per rectum and melena. He
denies fever and chills. He states that in the past, a physician told him he has mild anemia.
He had a recent cholecystectomy for recurrent gallstones and takes no medications.
He appears pale, icteric, and restless. Vitals signs are T 38.3 C (101.0 F), blood pressure
100/80 mm Hg, and pulse 120/min. Physical examination shows scleral icterus,
tachycardia with regular rhythm, no hepatosplenomegaly, and no fecal occult blood.
Differential Diagnosis
299
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
Acute hepatitis
1.
Acute hemolysis
2.
Autoimmune IgG hemolytic anemia
—
Cold agglutinin IgM disease
3.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
—
Hereditary red cell membrane deficiency with associated infection
—
Paroxysmal nocturnal hemoglobinuria (PNH)
4.
Cholangitis secondary to retained stone in common bile duct
5.
CBC
Peripheral smear
PT and PTT
LFTs
Urinalysis
U/S of abdomen
WBC 5,000/mm
3
(normal 4,500–11,000/mm
3
), hemoglobin 6 g/dL (normal 13–17 g/dL),
platelets 180,000/mm
3
(normal 150,000–350,000/mm
3
)
Peripheral smear bite cells present
PT and PTT time normal
Bilirubin 10 mg/dL (normal 0.2–1.2 mg/dL) 90% unconjugated; AST and ALT normal
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