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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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Test Results
Assessment
Heparin-induced thrombocytopenia (HIT) is defined as >50% drop in the platelet count after
several days of heparin use. HUS and TTP would also be associated with hemolytic anemia
and an elevated BUN or creatinine. ITP does not develop in response to the use of heparin;
however, ITP and HIT are both isolated decreases in the platelet count. ITP, however, causes
bleeding from a low platelet count, while HIT results in thrombosis from the ‘clumping’ of
platelets. HIT gives venous thromboses more often than arterial thromboses.
The diagnosis of HIT is very dependent on the temporal relationship of the start of heparin
with the timing of the drop in platelet count.
Further Management
Discontinue all heparin
Start argatroban or bivalirudin or fondaparinux
Stop warfarin
Repeat CBC
PT, aPTT, INR
Platelet count 54,000/mm
3
PT, aPTT, INR: normal
Serotonin release assay
Platelet factor 4 assay
Argatroban if renal failure present
Fondaparinux if liver failure present
351
CLINICAL PEARL
HIT causes >50% drop in platelets with heparin.
Discussion
HIT is increasingly recognized because of the increasing frequency of heparin use. If there is a
drop in platelet count >50%, then stop all heparin and switch to a direct-acting thrombin
inhibitor until there is no longer an indication for heparin.
You must not switch unfractionated heparin to low molecular weight heparin if HIT has
developed. Although HIT is less common with low molecular weight heparin, once the patient
develops HIT, all heparin products must be stopped.
When stimulated with serotonin, the platelets in a person with HIT will release labeled carbon.
This helps confirm the diagnosis of HIT.
Follow-up Management and Prevention
Causes clotting as a clinical manifestation; venous is 3x more common than arterial
clotting
Confirm with platelet factor 4 antibodies and serotonin release assay
Remove all heparins; do not switch to low molecular weight
Use argatroban or bivalirudin or fondaparinux as alternate therapy
Serotonin release assay is abnormal and platelet factor 4 antibodies are positive
Continue argatroban or fondaparinux or bivalirudin for 5 days
Oral anticoagulation for 6 months
352
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CLINICAL PEARL
Lepirudin and danaparoid are not available in the United States.
Final Diagnosis
Heparin-induced thrombocytopenia
Do not start warfarin until argatroban or fondaparinux or bivalirudin are started
Warfarin with INR 2-3 or rivaroxaban
353
Case 10
Chief Complaint
“I feel very weak and my urine is dark.”
History and Physical Examination
A 30-year-old woman is brought to the emergency department by her family because of the
development of profound weakness over a few days. She also has dark urine. She went to
see her family practice doctor who found blood on dipstick, but no red cells or white
cells were seen on microscopic examination. She is brought now to the hospital because
she developed left-sided weakness.
Upon examination blood pressure is 132/94 mm Hg, pulse 118/min, respirations 18 min,
and temperature 100.8 F. Neurologic exam reveals left-hand weakness, though it is
improved as compared to several hours ago. Cardiovascular exam reveals no murmurs.
Skin has a yellow discoloration. In HEENT, scleral icterus is found. The abdomen is soft.
Liver and spleen are normal.
Differential Diagnosis
Hemolysis
1.
Acute hepatitis
2.
Thrombotic thrombocytopenic purpura (TTP)
3.
Obstructive jaundice
4.
Stroke
5.
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Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
Assessment
Dark urine can be either hemoglobin or bilirubin. This patient has hemoglobin in the urine
turning it dark. The elevated total bilirubin with low direct means this is indirect or
unconjugated bilirubin. Unconjugated bilirubin is not water soluble and cannot go into the
urine. Unconjugated bilirubin is attached to albumin and does not filter.
This is not obstruction of the biliary system because obstruction gives an elevation of direct
bilirubin. Obstruction would also increase the alkaline phosphatase and GGT. Acute hepatitis
Paroxysmal nocturnal hemoglobinuria6.
CBC
LFTs
Urinalysis
Head CT
Chemistry 7
CBC: hematocrit 31%, platelets 42,000, WBC 7,500
LFTs: total bilirubin 5.2 mg/dL, direct 0.8 mg/dL, alk phos normal AST, ALT normal
Urinalysis: dip positive for blood, no cells seen; no bilirubin
Head CT: normal
Chemistry 7: BUN 34, creatinine 2.2 mg/dL
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elevates the ALT>AST. Drug-induced hepatitis such as from alcohol increases the AST>ALT
and the bilirubin is direct or water soluble from conjugation to diglucoronide.
This patient has hemolysis. In addition there is a low platelet count, renal dysfunction and
neurologic deficit. This is all consistent with thrombotic thrombocytopenic purpura (TTP).
Although there is no identifiable cause for TTP or HUS in the history it does not matter. Nearly
half of cases have no identified cause. TTP is a pentad of intravascular hemolysis, low
platelets, renal insufficiency, fever and neurologic problems. The absence of fever is not
especially relevant since it is rare for all 5 criteria to be present at the same time.
Further Management
Test Results
Discussion
CBC
Chemistry 7
LDH
Reticulocyte count
Peripheral smear
Normal saline
Plasmapheresis
CBC: Hematocrit 27%, Platelets 34,000, WBC 7,700
Chemistry 7: BUN 36, Creatinine 2.4 mg/dL
LDH: Elevated
Reticulocyte count: 7%
Peripheral smear: schistocytes and fragmented RBCs
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There is no single diagnostic test for TTP. TTP is diagnosed with a combination of the findings
such as we have here, which is evidence of intravascular hemolysis, low platelets, and renal
dysfunction. The single most characteristic feature is fragmented cells on the smear.
Schistocytes, helmet cells, and broken cells visible on routine blood smear are the main
confirmatory features. This leads to intravascular microangiopathic hemolytic anemia and can
cause stroke-like neurologic changes and acute glomerular renal injury.
The most common mistake or ‘wrong answer’ in TTP is to give platelets when the level goes
low. Giving platelets only makes TTP and HUS worse. The disorder is a deficiency of or
antibodies to a metalloproteinase (ADAMTS13) that breaks up VWF multimers. The multimers
accumulate on the endothelium and lead to physical shearing of RBCs and depletion of
platelets. If you give platelets they will only clog up the brain and kidney even more and
worsen the hemolysis.
The best treatment for TTP is plasma exchange and replacement with donor plasma
(plasmapheresis). They will remove anti-ADAMTS13 antibodies and replete ADAMTS13
levels.
CLINICAL PEARL
TTP results in intravascular hemolysis with fragmented cells on smear.
Increasing BUN and creatinine
Low platelets
Neurologic problems
Fever
Treat with plasmapheresis to replace ADAMTS-13
357
Follow-up Management and Prevention
Final Diagnosis
Thrombotic thrombocytopenic purpura (TTP)
Repeat CBC and kidney function every 1-2 hours at the beginning
Hematology consult
IV saline
Plasmapheresis (treatment of choice)
Do not transfuse RBCs or platelets
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7
Oncology
Case 1
Chief Complaint
“My right side is weak.”
History and Physical Examination
A 45-year-old woman comes to the emergency department because of a change in mental
status and hemiparesis of the right side. She was well until 2 weeks earlier when she
developed intermittent fevers and sore throat. She has suffered from several nosebleeds
and gum bleeding over the last week. Her local internist evaluated her earlier this
morning.
CBC shows WBC 1,500/mm
3
, hemoglobin 7.0 mg/dL, and platelets 17,000/mm
3
. She is
lethargic and is not moving her right side. Her T is 38.3 C (101.0 F) and BP is
160/100mm Hg. Examination of her eyes, ears, nose, and throat is normal. Her neck is
supple with no adenopathy. Her chest is clear, and her heart has a RRR with normal S1
and S2. There is no hepatosplenomegaly or peripheral edema noted. Neurologic
examination shows that she is confused, oriented x1, has right hemiparesis, and upgoing
359
toes on the right. She is uncooperative with sensory examination, but withdraws to painful
stimuli on the left.
Differential Diagnosis
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
Acute leukemia: myeloblastic or lymphoblastic
1.
Aplastic anemia
2.
Metastatic cancer
3.
Bone-marrow invasion by infection
4.
Myelodysplastic syndrome
5.
Peripheral smear
Blood cultures, UA, chest x-ray
Differential /absolute neutrophil count (ANC)
PT, aPTT, D-dimers, fibrin split products, fibrinogen
Head CT
Platelet transfusion
Meropenem, cefepime, or piperacillin/tazobactam IV
Smear: multiple immature myeloid cells (blasts) seen with atypical folding pattern; Auer
rods seen
Blood cultures: pending for 1–2 days
UA, chest x-ray normal
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