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Chapter 39 CHRONIC RENAL FAILURE AND DIALYSIS278
during the exchange procedure. The diagnosis is often suspected by the patient on the basis
of the new appearance of cloudiness of the dialysis effluent. Patients are instructed to seek
medical attention promptly when this occurs, and for this reason most episodes of peritonitis
are relatively mild. If the patient delays seeking medical attention, however, the symptoms
tend to become progressively more severe. Most patients have abdominal pain and
tenderness, but only a few have fever, nausea, vomiting, or even (at least early on) an elevated
peripheral white blood cell count. Localized peritoneal findings are suggestive of an acute
surgical abdomen rather than PD-associated peritonitis.
9. How is PD-associated peritonitis treated?
When fluid has been obtained from the effluent bag and laboratory studies have confirmed
the presence of a significant number of white cells (.100 cells/mm
3
with .50%
polymorphonuclear leukocytes) or a positive Gram stain, antibiotic treatment is initiated.
Commonly, vancomycin (30 mg/kg) is given intraperitoneally and may be repeated weekly.
Gram-negative coverage, with a third-generation cephalosporin, aztreonam, or an
aminoglycoside, can be added if thought appropriate. These may be given intraperitoneally as
well and should be followed by daily intraperitoneal maintenance doses as an outpatient.
Usually, each center has its own protocols for treatment, so the patient’s nephrologist or
dialysis nurse should be consulted. Follow-up should be in 48 hours, at which time cultures
and clinical findings are rechecked and therapy adjusted as necessary. Admission criteria
include severe pain, nausea and vomiting, a toxic appearance, or the inability of the patient to
comply with outpatient therapy and follow-up.
10. What are the indications for emergency dialysis?
Acute pulmonary edema, life-threatening hyperkalemia, or life-threatening intoxication or
overdose secondary to dialyzable toxins that ordinarily are excreted by the kidneys.
11. What is unique about a dialysis patient with cardiac arrest?
Two potentially reversible entities always should be considered in a CKD patient with cardiac
arrest:
n
Severe hyperkalemia may cause severe rhythm disturbances and ultimately cardiac arrest
without any other warning or clinical signs. When a patient suffers an arrest from whatever
cause, respiratory and metabolic acidosis and the efflux of potassium from cells can be
expected to produce hyperkalemia secondarily. In the patient who already may have a
tendency toward hyperkalemia, this further increase could cause the patient to be refractory
to standard advanced cardiac life support (ACLS) interventions. CKD patients in cardiac
arrest always should be given IV calcium if they do not respond immediately to the first
round of ACLS measures.
n
Acute pericardial tamponade may result from the accumulation of pericardial fluid or
spontaneous bleeding into the pericardial sac. Patients with tamponade tend to display
refractory hypotension or pulseless electrical activity, or both. Although less likely than
other entities to be the cause of refractoriness to resuscitation measures, the possibility of
pericardial tamponade always should be considered in patients in whom other measures
have failed. Bedside ultrasound may be diagnostic and emergency pericardiocentesis may
be life saving.
KEY POINTS: PD-ASSOCIATED PERITONITIS
1. Diagnosis: Cloudy dialysate effluent, abdominal pain, fever
2. Treatment: Typically with intraperitoneal antibiotics
Chapter 39 CHRONIC RENAL FAILURE AND DIALYSIS 279
12. What are the treatment options for acute pulmonary edema in patients
with CKD?
CKD patients with pulmonary edema do not have the ability to rid themselves of excess fluid
through the kidneys and ultimately require dialysis to correct volume overload. Most of the
interventions that are useful in patients with functioning kidneys also are useful in patients
with CKD while awaiting the initiation of acute dialysis. The patient should be given oxygen
and placed in a sitting position. Nitrates administered sublingually or intravenously are the
mainstay of temporizing therapy. Sublingual nitroglycerin can be given every 3 minutes to
decrease preload and afterload as blood pressure permits. IV nitroglycerin is a useful
alternative. IV morphine, although less popular, also may be helpful in decreasing pulmonary
venous hypertension, although patients may be more likely to require intubation and
mechanical ventilation because of its sedative action.
Dialysis is the definitive therapy and should be instituted as early as possible. The
PD patient with acute pulmonary edema presents a slightly different problem because
intensified dialysis, even with 4.25% glucose solution, is a slow means of removing fluid
and because the presence of 2 L of dialysate in the peritoneal cavity tends to have an
adverse effect on diaphragmatic excursion and pulmonary mechanics. Intubation and
mechanical ventilation may be necessary while continuing hourly exchanges of high-
concentration dialysate.
13. How should I treat hyperkalemia in a dialysis patient?
The approach is similar to that taken with nondialysis patients. IV calcium gluconate (10 mL
of a 10% solution) acts rapidly to antagonize the cardiotoxic effects of hyperkalemia (without
affecting the serum potassium level), but its effects last for only a few minutes. It should be
used only as a temporizing measure in patients with cardiovascular compromise or a widened
QRS complex on the electrocardiogram (ECG).
Nebulized albuterol (10 to–20 mg by inhalation) acts within a few minutes to shift
potassium into cells. It is easy to administer, generally has minimal side effects, and is
effective for a few hours. The dose can be repeated as necessary.
Glucose and insulin (typically 50 g and 0.1 units/kg, respectively, as a slow IV
infusion) also move potassium into cells but require close serial monitoring of blood
glucose levels.
IV sodium bicarbonate (50 mEq over 5 minutes) has a similar action but can exacerbate
volume overload and can acutely decrease the ionized calcium.
If dialysis is not immediately available to remove potassium from the body, sodium
polystyrene sulfonate (Kayexalate), a sodium-potassium exchange resin typically given orally
with sorbitol to enhance passage through the gut, can remove significant amounts of
potassium from the body. It is slow-acting, however, and should be reserved for situations in
which the patient is stable but requires continuing control of the serum potassium over hours,
until dialysis can be performed.
In all cases of acute hyperkalemia, the serum potassium level should be checked
frequently, and continuous ECG monitoring is mandatory until definitive treatment with
dialysis can be initiated.
KEY POINTS: INDICATIONS FOR EMERGENCY DIALYSIS
1. Acute pulmonary edema
2. Life-threatening hyperkalemia
3. Life-threatening intoxication or overdose with agents normally excreted by the kidneys
Chapter 39 CHRONIC RENAL FAILURE AND DIALYSIS280
14. What about air embolism?
Although air embolism has become rare with the advent of sophisticated monitoring and
alarm systems on hemodialysis machines, when it does occur it is often a devastating event
and one for which the patient almost surely will be brought to the nearest ED.
Air embolism should be suspected when a patient experiences a sudden acute
decompensation during the course of a hemodialysis treatment. Several immediate
measures are thought to be helpful. Any IV lines should be clamped. The patient should be
given 100% oxygen and laid on the left side with the head down, in an attempt to cause the
air to collect at the apex of the right ventricle. At this point, if the patient is reasonably
stable, an interventional radiologist or cardiologist can be consulted for consideration of
passage of a central venous catheter into the right ventricular apex, allowing the air to be
aspirated directly out of the heart. For patients who are in close proximity to a hyperbaric
chamber, treatment with 100% oxygen at several atmospheres can shrink the size of the
bubbles and enhance resorption of the gas. One should be certain before embarking on this
course, however, that the patient’s symptoms are due to air embolism rather than, for
example, a sudden spontaneous pneumothorax.
15. How should a patient with acute shortness of breath be evaluated?
The rule of thumb is to dialyze CKD patients who are short of breath because volume overload
is the most common cause. It is sometimes difficult to make the diagnosis of volume
overload. The patient’s weight may be the best guide. Physical examination is not always
helpful, and chest radiographs may be misleading.
16. What are the main differential diagnostic considerations for chest pain
in CKD?
Always think first of either angina or pericarditis. Some patients with CKD, particularly
those who are anemic, may have angina and cardiac ischemia even if a previous cardiac
catheterization has shown a noncritical coronary obstruction. This is due to increased cardiac
oxygen demands and decreased oxygen delivery to the heart. Although cardiac enzyme levels
may be altered in CKD, renal failure does not obscure the usual ECG and enzyme changes of
acute myocardial infarction.
17. What is the differential diagnosis of hypotension in a patient with end-stage
renal disease (ESRD)?
The most common entities are hypovolemia after dialysis, sepsis, hemorrhage, and acute
pericardial tamponade.
KEY POINTS: TREATMENT OF HYPERKALEMIA
1. IV calcium
2. Inhaled albuterol
3. IV glucose and insulin
4. IV sodium bicarbonate
5. Oral or rectal Kayexalate
6. Dialysis
Chapter 39 CHRONIC RENAL FAILURE AND DIALYSIS 281
18. What are the major causes of altered mental status in patients with ESRD?
Dysequilibrium syndrome, caused by rapid solute shifts during hemodialysis, is a
consideration, but a major pitfall is to attribute every change in mental status to this entity.
Drug effects are a major cause of altered mental status, as is spontaneous intracranial
hemorrhage. Any patient with localizing signs should have a computed tomography (CT) scan
of the head; patients without localizing signs should also undergo CT scanning, however,
because subdural hematoma may not cause focal findings.
BIBLIOGRAPHY
1. Aronoff GR, Bennett WM, Berns JS, et al: Drug prescribing in renal failure: dosing guidelines for adults, ed 5,
Philadelphia, 2007, American College of Physicians.
2. Piraino B, Bailie GR, Bernardini J, et al: Peritoneal dialysis-related infections. Recommendations: 2005. update.
Perit Dial International 25:107–131, 2005.
3. Wolfson AB: Chronic kidney disease and dialysis-related emergencies. In Wolfson AB, Hendey GW, Ling LJ,
et al, editors: Harwood-Nuss’ clinical practice of emergency medicine, ed 5, Philadelphia, 2010, Lippincott
Williams & Wilkins, pp 623–628.
4. Wolfson AB: Renal failure. In Marx JA, Hockberger RS, Walls RM, et al, editors: Rosen’s emergency medicine:
concepts and clinical practice, ed 7, Philadelphia, 2010, Mosby, pp 1257–1281.
KEY POINTS: MOST COMMON CAUSES OF HYPOTENSION
IN DIALYSIS PATIENTS
1. Hypovolemia after dialysis
2. Sepsis
3. Hemorrhage
4. Pericardial tamponade
283
HEMOSTASIS AND COAGULOPATHIES
CHAPTER 40
Thomas B. Barry, MD and Kathryn Getzewich, MD
IX. HEMATOLOGY/ONCOLOGY
1. What is meant by hemostasis?
Hemostasis is a balance between excessive bleeding and thrombosis. It is the active process
of clot formation and degradation in response to injury of a blood vessel. This response
normally occurs through the coordinated efforts of the blood vessel endothelium, platelets, the
clotting factor cascade, and fibrinolysis.
KEY POINTS: THREE PHASES OF HEMOSTASIS
1. Platelet plug formation
2. Propagation of the coagulation cascade and fibrin clot formation
3. Balanced fibrinolysis
2. Is hemophilia the main cause of hemostatic abnormality?
Most hemostatic abnormalities result from drugs such as heparin, warfarin, and aspirin or
from associated disease such as liver or kidney failure. The hemophilias are important but less
common.
3. Do I really need to know the whole clotting cascade to manage patients?
A working knowledge should include the basics of the three phases of hemostasis, some key
clotting factors, and familiarity with basic testing and therapeutics.
n
In primary hemostasis, after injury, platelets and von Willebrand factor (vWF) from the
endothelium interact to form a plug (platelet adhesion). Platelet activation and aggregation
occur along with vessel constriction. Disorders include problems with platelet quantity and
function, as well as vWF problems and vascular abnormalities such as hereditary
telangiectasia. Platelet count and bleeding time are used to assess this phase of hemostasis.
n
In secondary hemostasis, the platelet plug is reinforced with cross-linked fibrin from the
coagulation cascade (factor XIII causes covalent cross-links). Effective functioning of the
cascade may be impaired by deficiencies of coagulation factor activity (hemophilia A and B)
or by inadequate factor production such as with warfarin use.
n
In tertiary hemostasis, the fibrin clot is enzymatically broken down by plasmin. Endothelial
cells release plasminogen activator, which converts plasminogen to plasmin. The plasmin
breaks down fibrin and fibrinogen into fibrin split products and D-dimers. Excessive
fibrinolytic activity or deficiencies of fibrinolytic inhibitors can increase bleeding. Because
protein C and protein S are involved in the regulation of blood clotting, deficiencies can
result in excessive intravascular clotting.
4. What are the intrinsic and extrinsic coagulation pathways? How can I tell the
difference?
Prothrombin time (PT) is affected by the extrinsic (and common) pathways of the coagulation
cascade and partial thromboplastin time (PTT) by defects in the intrinsic (and common) paths.
Chapter 40 HEMOSTASIS AND COAGULOPATHIES284
The extrinsic pathway is activated by tissue factor exposed at the site of injury. The intrinsic
pathway is initiated by blood exposure to a negatively charged surface. A patient with a
prolonged PTT and a normal PT is considered to have a defect in the intrinsic coagulation
pathway. The name indicates that all of the components of the PTT test (except kaolin) are
intrinsic to the plasma. On the other hand, a patient with a prolonged PT and a normal PTT has
a defect in the “extrinsic” coagulation pathway (tissue factor being extrinsic to the plasma).
Prolongation of both the PT and the PTT implies that the defect is in a common pathway. Both
pathways converge to activate factor X, which activates prothrombin to thrombin.
5. What parts of the history and physical can help me assess a suspected
bleeding abnormality?
It is important to ask about medications, previous medical history (especially liver, kidney, and
malignant disease), previous problems with bleeding (such as with surgeries and dental work),
and family history of bleeding disorders. In patients with known bleeding disorders, ask about
the nature of their disease and previous therapies. They are frequently knowledgeable about
their individual disease. Platelet disorders frequently result in petechia, purpura, epistaxis,
and gum and other mucosal bleeding. They are common in women and usually acquired as
opposed to congenital. Problems with coagulation are more commonly congenital, found more
often in men, and are likely to present as deep muscle or joint bleeding. Coagulopathy is rarely
the cause of epistaxis, menorrhagia, or gastrointestinal (GI) bleed.
6. How do I interpret PT, PTT, and international normalized ratio (INR)?
PT tests the factors of the extrinsic and common pathways. It is prolonged by deficiencies of
prothrombin, fibrinogen, and factors V, VII, and X. A PT 2 seconds more than the control is
significant. PTT tests all the intrinsic and common pathways, including all factors except VII
and XIII. INR reduces interlaboratory variation by indexing thromboplastin test lot activity to
an international standard. Liver disease, warfarin use, and other abnormalities of the vitamin K
sensitive factors (i.e., II, VII, IX, X) affect the PT and INR. INR of 1 is normal. An INR between
2 and 3 indicates a therapeutic level of warfarin.
7. What are the causes of thrombocytopenia?
n
Decreased production: Marrow disease, chemotherapy, alcohol or thiazide effect
n
Immune destruction: Idiopathic thrombocytopenic purpura (ITP), systemic lupus
erythematosus (SLE), lymphoma, quinine, quinidine, and postinfectious disease
n
Toxic destruction: Disseminated intravascular coagulation (DIC), thrombotic
thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), hemolysis with
elevated liver enzymes and low platelets (HELLP) syndrome
n
Splenic sequestration (hypersplenism; rare): Hematologic malignancy, portal hypertension,
autoimmune hemolytic anemia, hereditary spherocytosis
n
Dilution: Massive transfusion
n
Lab error: It happens. “I’m shocked, shocked. . . .” (Claude Rains, Casablanca, Warner
Brothers, 1942)
8. What are the differences between idiopathic and chronic thrombocytopenic
purpura?
n
ITP should be a diagnosis of exclusion after considering SLE, antiphospholipid syndrome,
HIV, and lymphoproliferative disorders. It is associated with antiplatelet antibody
immunoglobulin G (IgG). The acute form is seen in children 4 to 6 years old several weeks
after a viral prodrome. It is self-limited with a 90% rate of spontaneous remission. Morbidity
and mortality rates are low, and steroid therapy does not seem to alter the course.
n
Chronic ITP is found in adults. It is three times more common in women than men.
Severity waxes and wanes with only a 1% mortality, but spontaneous remission is rare. It
may respond to therapy with glucocorticoids, intravenous (IV) immunoglobulin, and
splenectomy if recurrent. Other treatments include plasmapheresis, androgen therapy with
danazol, cyclophosphamide, azathioprine, vincristine, thrombopoietin, antiCD40 ligand,
rituximab, and anti-D immunoglobulin (WinRho) in Rh-positive presplenectomy patients.
Chapter 40 HEMOSTASIS AND COAGULOPATHIES 285
Platelet transfusion is reserved for life-threatening bleeds because it may increase
antiplatelet antibodies.
9. What are the five clinical signs of TTP?
Only 40% of patients have all five:
n
Fluctuating change in mental status
n
Thrombocytopenia
n
Fever (in 90% of patients)
n
Microangiopathic hemolytic anemia
n
Renal impairment
10. What causes TTP? Is it worse than ITP?
TTP results from subendothelial and intraluminal deposits of fibrin and platelet aggregation
in capillaries and arterioles. Prostacyclin and abnormal platelet aggregation are thought to
contribute to its origins. It may affect patients of any age or gender, although most are 10 to
40 years old and 60% are female. When untreated, there is 80% mortality at 3 months as a
result of microthrombi in the heart, brain, and kidneys. Recently plasmapheresis has reduced this
to 17%. Other therapies include steroids, splenectomy, a-globulin, vincristine, and antiplatelet
agents such as aspirin and dipyridamole (Persantine). Platelet transfusions may cause additional
microcirculatory thrombi and should be avoided unless bleeding is life-threatening.
11. What is hemolytic uremic syndrome (HUS)?
HUS is similar to TTP in that they both present with hemolytic anemia, fever, neurologic
abnormality, and renal dysfunction. However, HUS causes less change in mental status and
more renal dysfunction. Patients with HUS tend to be younger (children are more common
than adults), and onset is often associated with a bacterial gastroenteritis such as Escherichia
coli O157:H7 and Shigella spp.
12. Should I worry about thrombocytopenia during a large-volume blood
transfusion?
Stored banked blood is platelet poor because platelets have a life span of only 9 days. Follow
platelet counts after 10 units of blood. Transfuse platelets when the count is down to 50,000/mL.
13. How does aspirin increase bleeding?
Aspirin blocks cyclooxygenase, which decreases thromboxane formation leading to decreased
platelet aggregation and less vasoconstriction. Aspirin poisons this reaction for the life of the
platelet. Nonsteroidal anti-inflammatory drugs, such as indomethacin, have this effect only
while in the circulation. Uremia has a similar reversible effect.
14. What are the indications for platelet transfusions?
As previously noted, platelet transfusion should be delayed in ITP and TTP to avoid disease-
specific complications and alloimmunization. It is more commonly indicated for primary bone
marrow problems. In a patient with a platelet count greater than 50,000/mL, hemorrhage due
to the deficiency is unlikely. From 10,000 to 50,000/mL there is variable risk with trauma,
ulcer, and invasive procedures. Choosing when to transfuse at these levels is not an exact
science. Platelet transfusion is indicated with counts less than 10,000/mL because there is a
significant risk of spontaneous hemorrhage. Each bag of random donor platelets may be
expected to raise the platelet count 5,000/mL. They are usually ordered six at a time.
15. What is the most common inherited bleeding disorder?
It is von Willebrand’s disease (5–10 cases per million population). It is usually autosomal
dominant. There is a deficiency or dysfunction of vWF and a mild factor VIII defect. Treatment
is with desmopressin in the mild, most common, type I form of the disease.
In more severe types, therapy is with cryoprecipitate based on the patient’s factor VIII
level. Usual dose is one to two bags/10 kg. In von Willebrand’s this is found to stimulate
factor VIII activity and less is needed in redosing.
Chapter 40 HEMOSTASIS AND COAGULOPATHIES286
16. Do people with hemophilia A have low levels of factor VIII?
It is the activity of factor VIII that is impaired, technically not its level. Seventy percent of
cases are transmitted by sex-linked recessive (X chromosome) inheritance; 30% of cases are
due to spontaneous mutation. Severe disease has less than 1% activity, and spontaneous
bleeding (joints, deep muscles, urinary tract, and central nervous system [CNS]) is a problem.
Between 1% and 5% activity is classified as moderate disease with problems occurring mostly
after trauma and surgery. Above 5% is mild disease, but some trauma and surgical risks
persist. PTT is only prolonged with less than 35% activity.
Pearl: 1 unit of factor VIII per kilogram increases the activity level by 2% (unless
adversely affected by anti-factor VIII antibodies (IgG), which develop in 7% to 20% of
patients). Recombinant DNA factor VIII is the replacement of choice and lacks the hepatitis B,
C, and HIV risks of fresh frozen plasma (FFP) and cryoprecipitate.
17. How is factor VIII dosed in hemophilia A?
Twenty-five units per kilogram for moderate bleeding, 50 units/kg for severe hemorrhage or
life-threatening bleeding site (GI, neck, sublingual, retroperitoneal, intra-abdominal, head
injury, CNS bleed, and necessary surgical procedures). Because the half-life is 8 to 12 hours,
redose with half the loading dose after 8 to 12 hours. Recombinant factor VIII unit
concentration is noted on the label. Cryoprecipitate (from FFP) is assumed to be 80 to
100 units of factor VIII per bag.
18. What is Christmas disease?
Hemophilia B, which involves decreased factor IX activity. The clinical presentation is the same
as hemophilia A. The genetic pattern is the same, although less prevalent in the population
with only
1
⁄5 the number of cases. Treatment is with factor IX, 50 U/kg or FFP.
Pearl: There is no factor IX in cryoprecipitate.
19. What does desmopressin (DDAVP) do?
DDAVP is a synthetic analog of antidiuretic hormone. It works by causing release of vWF from
endothelial storage sites and increases levels of factor VIII in hemophilia A and some cases of
von Willebrand’s. The dose is 0.3 mg/kg IV; it lasts 4 to 6 hours and is most effective in mild
to moderately deficient patients.
20. What factors are affected by vitamin K deficiency? Warfarin? Liver disease?
Banked blood?
n
Vitamin K deficiency affects II, VII, IX, and X, the same ones affected by warfarin.
n
Hepatic insufficiency affects all factors except VIII.
n
Stored blood is low in V, VIII, and platelets.
KEY POINTS: HEMOSTATIC DEFICIENCIES
1. With hemophilia A and B, the bleeding time is normal (as is the PT and the PTT in mild and
moderate cases).
2. Bleeding time is increased with von Willebrand’s disease.
3. PT reflects extrinsic pathway abnormality through factor VII deficient activity.
4. Factor VII has the shortest half-life of the factors (3–5 hours) and causes the first manifesta-
tions of production deficiency.
5. An INR of 2–3 is recommended with most warfarin therapy.
6. Deficiency of factors VIII, IX, and XI account for 99% of inherited bleeding disorders. If
congenital bleeding disorder is suspected, FFP at 15 mL/kg will support hemostasis while
a definitive diagnosis is being made.
Chapter 40 HEMOSTASIS AND COAGULOPATHIES 287
21. What happens in DIC?
Platelets and clotting factors (especially V, VIII, and XIII) are consumed. Thrombin formation
overwhelms fibrinolysis and activates fibrinogen. Fibrin is deposited in small vessels of
multiple organ systems. Fibrin degradation products are released, and platelet function, as
well as fibrin polymerization, are decreased.
Treatment is with platelets and FFP. Heparin may be used if fibrin deposition and
thrombosis dominate the clinical picture.
22. What are heparin-induced thrombocytopenia (HIT) and heparin-induced
thrombocytopenia with thrombosis (HITT)?
HIT type I is a nonimmune-mediated thrombocytopenia that usually resolves without
treatment or complication. The more serious HIT type II (the form usually referred to when
discussing HIT) is caused by antibodies to heparin/platelet factor 4 complex. It results in
platelet activation and clot formation. It usually occurs 5 to 10 days after exposure to heparin
but may occur after as few as 10 hours. It occurs in 2% of patients on unfractionated heparin
anticoagulation therapy and less commonly with low-molecular-weight heparin. Platelet
counts drop to 50,000 to 100,000/mL. HITT develops in 50% of the patients with HIT. HIT
and HITT require discontinuation of heparin (including heparin flushes). Prophylactic platelet
transfusions should be avoided. A direct thrombin inhibitor is indicated in patients with
thrombosis (i.e., lepirudin or argatroban). Doppler ultrasound of the legs is indicated in HIT
because recent studies have found subclinical deep venous thrombosis (DVT) in up to 50% of
HIT patients.
23. Need help with HELLP?
HELLP criteria:
n
Microangiopathic hemolytic anemia
n
Serum aspartate transaminase levels greater than 70 U/L
n
Platelets less than 100,000/mL
The HELLP syndrome is a form of preeclampsia. Gestational thrombocytopenia (100,000–
150,000/mL) is found in 5% to 10% of third trimester pregnancies. It is even more common
in pregnancies complicated by preeclampsia (15%–20%) and eclampsia (40%–50%). Fetal
and maternal mortality are increased. Treatment is primarily supportive, although platelet
transfusion may be required prior to cesarean section. DIC may develop.
24. How do heparin and low-molecular-weight heparin (LMWH) work?
Heparin catalyzes the inactivation of thrombin and factor X by antithrombin. It also has some
effect on factors II, IX, and XI. Factor VII is not affected. At usual doses, it will prolong the
PTT (and thrombin time [TT]) but not the PT. Occult GI bleeding is a relative contraindication
to its use, and clearance is prolonged in hepatic and renal dysfunction.
LMWH is derived from smaller pieces of the heparin molecule. Weight-based
subcutaneous dosing of LMWH without anticoagulation monitoring has proven safe and
effective in clinical trials. (This is fortunate, because LMWH inactivates factor X more than it
does thrombin, so PTT is not significantly affected and cannot/need not be used to monitor
clinical effect and therapeutic plasma concentrations.) Weight-based pharmacokinetic
predictions for LMWH are not reliable in patients weighing more than 100 kg, pregnant
patients, and those with decreased creatinine clearance. If LMWH is used in these patients,
anti-X activity must be monitored. Unfractionated heparin often becomes the drug of choice in
these patients.
25. How do I treat hemorrhage secondary to heparin therapy?
With major bleeding episodes, heparin can be 100% reversed with protamine sulfate at a dose
of 1 mg/100 U of circulating heparin to a maximum dose of 250 mg. It is given slowly,
intravenously, over 10 minutes. Rapid infusion increases the risk of anaphylaxis. Protamine is
only 60% effective in reversing LMWH, so unfractionated heparin is usually preferred in cases
when surgery or invasive procedures are likely.