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488

N. Amin and V. Patil

 

 

Step 8: Use less allergenic blood products

In patients with multiple blood transfusion and transfusion-related complications, alternatively processed blood products should be considered (Table 61.1).

Step 9: Consider threshold for blood transfusion

If the bleeding has stopped and serum lactate is normal, do not transfuse any more blood or blood products.

In the absence of active bleeding, keep a transfusion threshold of less than 7.0 g% and keep 7–9 g/dL Hb in critically ill patients who are hemodynamically stable.

RBC transfusion may be beneficial in anemic patients with acute coronary syndrome (keep Hb >10 g/dL).

Step 10: Use blood products judiciously

In the absence of bleeding, do not correct high INR with FFP.

Patients having inadequate intake or on anticoagulants and broad-spectrum antibiotics are likely to have vitamin K deficiency, which can cause deranged INR.

They will benefit from intravenous vitamin K supplementation.

Suggested Reading

1.Napolitano LM, Kurek S, American College of Critical Care Medicine of the Society of Critical Care Medicine, Eastern Association for the Surgery of Trauma Practice Management Workgroup. Clinical practice guideline: red blood cell transfusion in adult trauma and critical care. Crit Care Med. 2009;37:3124–57.

These are evidence-based guidelines on the use of RBC transfusions in adult trauma and critical care endorsed by SCCM.

2.Klein HG, Spahn DR. Series on transfusion medicine. Lancet. 2007;370:415–48.

An excellent review on red cell transfusion, platelet transfusion, and coagulation factor concentrates.

3.BCSH. Guidelines for management of massive blood loss. Br J Haematol. 2006;135:634–41.

It is an evidence-based guideline on management of massive blood loss.

Websites

1.www.transfusionguidelines.org.uk

2.www.asahq.org/publicationsAndServices/transfusion.pdf

3.www.bcshguidelines.com

Disseminated Intravascular Coagulation

62

and Thrombocytopenia

Vijaya Patil, Nayana Amin, Reshma Ambulkar,

and Atul Kulkarni

A 40-year-old male patient was admitted with acute pancreatitis. He developed fever, tachycardia, hypotension, and respiratory distress on the third day of admission. His abdomen was severely tender and distended. Next morning the nurse noticed excessive oozing from arterial and central line insertion site, and his abdomen was further distended.

Bleeding manifestation due to disseminated intravascular coagulation (DIC) occurs in 1% of hospital admission. Assessing and managing these patients require a systematic approach as DIC is a reflection of underlying systemic disease affecting the coagulation system, resulting in procoagulant activation, fibrinolytic activation, consumption coagulopathy, and end organ damage, which needs to be recognized and treated.

Step 1: Initial resuscitation

Special emphasis should be placed on stabilizing hemodynamics, and if needed, blood and blood product transfusion should be started.

Care should be taken in establishing venous access in actively bleeding patients who may be coagulopathic.

Peripheral access is preferable to central.

Use ultrasound-guided venous cannulation if possible and preferably choose compressible sites like internal jugular or femoral vein.

Avoid arterial punctures.

V. Patil, M.D. (*) • N. Amin, M.D. • R. Ambulkar, M.D., F.R.C.A. • A. Kulkarni, M.D. Department of Anaesthesia, Critical Care & Pain, Tata Memorial Hospital,

Mumbai, India

e-mail: vijayappatil@yahoo.com

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

489

DOI 10.1007/978-81-322-0535-7_62, © Springer India 2012

 

490

V. Patil et al.

 

Table 62.1 Conditions associated with DIC

Infections

Bacterial—Gram-negative and Gram-positive sepsis

 

Viral—cytomegalovirus, HIV, hepatitis, dengue

 

Fungal

 

Parasitic—malaria, leptospirosis

Malignancy

Solid tumors

 

Hematological—acute promyelocytic leukemia is

 

commonly associated with DIC

Obstetric

Amniotic fluid embolism

 

Placenta abruption

 

Preeclampsia

 

Intrauterine fetal death/retained products of conception

Toxic and immunological insults

Viper snake bites

 

Massive transfusion

 

ABO transfusion incompatibility

 

Transplant rejection

Massive inflammation

Severe trauma

 

Crush injuries

 

Massive burns

 

Fulminant liver failure

 

Severe hypo-/hyperthermia

 

Severe pancreatitis

Vascular disorders

Aortic aneurysms

 

Giant hemangiomas

Step 2: Take relevant history and perform focused physical examination

Take history of known systemic conditions associated with DIC and coagulation disorders (Table 62.1).

Review the drug history, particularly the use of heparin and warfarin, and consumption of antiplatelet agents including nonsteroidal anti-inflammatory drugs.

Look for bleeding manifestation, superficial like skin and mucosal (petechiae, purpura) or visceral and deep seated (gastrointestinal bleeding).

Look for thrombotic manifestations like deep vein thrombosis (DVT) of lower limbs or venous or arterial thrombosis at any other site (e.g., cerebral).

Step 3: Investigate to ascertain the type and cause of bleeding (Table 62.2)

Complete blood count, including platelet count and peripheral smear, for the presence of fragmented RBCs.

Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT).

Fibrinogen level, fibrin degradation product (FDP), D-dimer.

Renal and liver function tests.

The commonest laboratory abnormality is thrombocytopenia followed by elevated FDPs, prolonged PT, prolonged APTT, and a low fibrinogen.

Table 62.2 Coagulation profile

 

 

Test

What does it monitor

Normal value

Inference

Prothrombin time

Factors that are in the extrinsic

11–13 s

Prolongation of the PT is most often a result of deficiencies in factor

 

pathway and common pathway:

 

VII but can also be caused by any of the extrinsic and common

 

factors VII, X, V, and II

 

pathway factors. Decreased fibrinogen, levels less than 100 mg/dL,

 

 

 

will also prolong the PT

 

 

 

Cholestatic jaundice

 

 

 

Acute or chronic liver failure

 

 

 

DIC

 

 

 

Malabsorption

 

 

 

Vitamin K deficiency

 

 

 

Coumadin (warfarin) therapy

 

 

 

Factors I, II,V, VII, X deficiency

Activated partial

Factors that are designated in the

28–34 s

Heparin therapy

thromboplastin time

intrinsic pathway: factors XII, XI,

 

Factor deficiency

 

IX, VIII, X, V, II, and fibrinogen

 

Presence of an inhibitor like lupus anticoagulants

 

 

 

Platelet count

Quantifies platelet number

130–400 × 109/L

Decreased production (bone marrow disorder), increased destruction,

 

 

 

idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocy-

 

 

 

topenic purpura, sequestration (hypersplenism)

Thrombin time

Evaluates the last step of

13–15 s

Heparin therapy

 

coagulation (conversion of

 

DIC

 

fibrinogen to fibrin)

 

Qualitative fibrinogen abnormalities or hypofibrinogenemia

 

 

 

 

 

 

Elevated FDPs (fibrin degradation products)

Fibrinogen level

 

200–500 mg/dL

Congenital and acquired hypofibrinogenemia

 

 

 

DIC

D-dimer

Cross-linked D fragments of the

500 ng/mL

Deep venous thrombosis, DIC, pulmonary embolism, thrombolytic

 

protein fibrinogen

 

treatment, postoperative

Thrombocytopenia and Coagulation Intravascular Disseminated 62

491

492

V. Patil et al.

 

 

 

 

Table 62.3 ISTH diagnostic

 

 

 

Platelet count

 

 

scoring system for DIC

>100 × 109/L

0

 

 

<100 × 109/L

1

 

 

<50 × 109/L

2

 

 

Fibrin marker (e.g., D-dimer, FDP)

 

 

 

No increase

0

 

 

Moderate increase

2

 

 

Strong increase

3

 

 

Prolonged PT

 

 

 

<3 s

0

 

 

>3 but <6 s

1

 

 

>6 s

2

 

 

Fibrinogen level

 

 

 

>1 g/dL

0

 

 

<1 g/dL

1

 

D-dimer, FDP, and antithrombin levels can be used for rapid and specific diagnosis of DIC, with antithrombin providing an indicator for severity and prognosis.

Diagnosis of DIC is essentially confirmed by demonstrating increased thrombin generation (decreased fibrinogen) and increased fibrinolysis (elevated D-dimer or FDP).

Step 4: Ascertain severity and prognosticate outcome

Calculate the DIC score (Table 62.3) with the ISTH (International Society of Thrombosis and Haemostasis) scoring system which provides objective measurement of DIC and correlates with outcome.

Step 5: Continue resuscitation

Continue resuscitation and maintain hemodynamic stability using crystalloids and/or colloids.

In colloids, preferably use gelatins as they do not interfere with clotting.

If you are using starches, use tetrastarch preferably, as they have less effect on the coagulation profile, but do not exceed maximum dose (50 mL/kg/day).

Step 6: Correct coagulopathy (see Table 61.2 in Chap. 61)

Repeat the coagulation profile and complete blood count frequently and replace blood and blood products.

In the presence of ongoing blood loss, try to normalize prothrombin time and APTT and aim to maintain platelet count of more than 50,000.

Do not use antifibrinolytic agents as they may aggravate thrombosis.

Patients who have DIC with a primary hyperfibrinolytic state and who have severe bleeding can be treated with lysine analogues, such as tranexamic acid (e.g., 1 g every 8 h).

There is no role of heparin in actively bleeding patients.

62 Disseminated Intravascular Coagulation and Thrombocytopenia

493

 

 

It should be considered only where thrombosis predominates such as arterial or venous thromboembolism or severe purpura fulminans associated with vascular skin infarction.

Step 7: Treat the underlying disorder

Repeat the tests to monitor the dynamically changing scenario and continue treatment based on clinical observation and laboratory results.

Once patient stops bleeding, do not try to correct laboratory abnormalities as transfusion of blood and blood products should be based on clinical condition and bleeding rather than laboratory values only.

Calculate score

More than 5 overt DIC: repeat score daily.

Less than 5 suggestive for nonovert DIC: repeat for the next 1–2 days.

Thrombocytopenia

A 50-year-old male patient was admitted with acute pancreatitis. His blood investigations showed Hb 10.7 g%, WBC 12,000/mm3, and platelets 110,000/ mm3. On the third day, he worsened clinically. His WBC count was 20,000/mm3 and platelets were 70,000/mm3. However, the next day, he further deteriorated requiring inotropes and ventilatory support. His Hb dropped to 6.4 g%, WBC count rose to 28,000 mm3, and platelets further dropped to 40,000/mm3.

Step 1: Resuscitate

Resuscitate, monitor, and stabilize in the ICU (refer to Chap. 78). In patients with low platelets and coagulopathy, ultrasound-guided jugular venous catheter insertion for fluid resuscitation should be performed.

Send blood for peripheral blood smear, grouping, cross-matching, coagulation profile, and biochemistry.

Step 2: Assess severity of thrombocytopenia

Thrombocytopenia is defined as a platelet count less than 150 × 109/L.

In critically ill patients, a threshold of less than100 × 109/L may be taken.

The ability to form a hemostatic plug is retained until the platelet count drops to less than 100 × 109/L

Step 3: Assess cause of thrombocytopenia (Table 62.4)

Careful history, physical examination, previous medical records, and current chart review usually reveal the cause of low platelet count.

Ask about bleeding from other sites in past, for example, frequent nosebleeds, gum bleeds, melena, hemoptysis, and blood in stool or urine.

494

V. Patil et al.

 

Table 62.4 Causes of thrombocytopenia

Pseudothrombocytopenia seen in

EDTA causes in vitro clumping of platelets. Presence of

asymptomatic patients

platelet clumps in the peripheral smear and a normal repeat

 

platelet count in citrated blood confirm pseudothrombocy-

 

topenia. In some patients, automated blood reports show

 

thrombocytopenia due to presence of giant platelets that are

 

counted as RBCs in automated machines; however, manual

 

platelet count is normal

Dilutional thrombocytopenia

Massive blood transfusion

Ambulatory patients

ITP

 

Drug-induced—chemotherapy, miscellaneous drugs

 

Infections—Epstein–Barr virus (EBV), HIV, others

 

Connective tissue disorders—rheumatoid arthritis, systemic

 

lupus erythematosus (SLE), antiphospholipid antibody

 

syndrome

 

Hypersplenism

 

Primary marrow disorder

Acutely ill patients

Infection/sepsis

 

DIC

 

TTP-HUS

 

Posttransfusion purpura

Pregnant patient

Gestational (platelet count >70 resolves after pregnancy)

 

ITP

 

HELLP—hemolysis, elevated liver enzymes, low platelets

Cardiac patients

HIT

 

Cardiac bypass

 

Dilutional

 

Gp IIb/IIIa inhibitor-related

 

TTP related to clopidogrel or ticlopidine

Patient with thrombosis

HIT

 

Antiphospholipid antibody syndrome

 

Paroxysmal nocturnal hemoglobinuria

History of previous platelet counts.

History of previous blood or platelet transfusion.

Medication history and review medication chart—particularly, use of heparin, warfarin, and antiplatelet agents including nonsteroidal anti-inflammatory drugs (Table 62.5).

Heparin-induced thrombocytopenia (HIT) should be considered if the platelet count decreases by 50% and/or thrombosis occurs 5–14 days after starting heparin.

History of known systemic conditions associated with defects in platelets like alcoholism, cirrhosis, HIV infection, systemic lupus erythematosus (SLE), and uremia.

Family history of excessive bleeding.

62 Disseminated Intravascular Coagulation and Thrombocytopenia

495

 

 

 

Table 62.5 Drugs associated with thrombocytopenia

 

 

Mechanism

 

Drugs

 

 

 

Drug-specific antibody

 

H2 receptor blockers

Ranitidine, cimetidine

 

 

 

Gp IIb/IIIa inhibitors

Abciximab

 

Drug-dependent antibody

Antibiotics

Vancomycin, rifampicin,

 

 

 

 

 

chloroquine, amphotericin B,

 

 

 

 

 

sulfonamides

 

 

 

Salicylates/NSAIDs

Aspirin, diclofenac, ibuprofen

 

 

 

Antiepileptics

Valproate, carbamazepine,

 

 

 

 

 

phenytoin

 

 

 

Antiarrhythmics

Amiodarone

 

 

 

Miscellaneous

Quinine, furosemide, thiazide,

 

 

 

 

 

morphine

 

Hapten-dependent antibody

Antibiotic

 

Penicillin, some cephalosporins

 

Induction of autoantibodies

Antiarrhythmics

Procainamide

 

 

 

Miscellaneous

Gold salts

 

Myelosuppression

 

Antibiotics

Linezolid

 

 

 

Chemotherapeutic agents

 

 

Unknown

 

Antibiotics

Fluconazole, daptomycin,

 

 

 

 

 

ganciclovir, nitrofurantoin,

 

 

 

 

 

piperacillin

 

 

 

Miscellaneous

Digoxin, haloperidol

 

 

 

Gp IIb/IIIa inhibitors

Eptifibatide

 

Immune complex with PF4

Heparins

 

Unfractionated and low-molecular-

 

 

 

 

weight heparin

 

Interference with folate

Antibiotic

 

Meropenem

 

metabolism

 

 

 

 

 

Thrombotic microangiopathy

 

 

Clopidogrel, ticlopidine

 

Preexisting antibodies

 

 

 

Abciximab

 

Table 62.6 Factors associated with platelet refractoriness

 

 

Nonimmune factors

Clinical factors

Splenomegaly, fever, infection, bleeding, dissemi-

 

 

 

 

nated intravascular coagulation

 

 

Drugs

 

Amphotericin B, vancomycin, ciprofloxacin, heparin

 

Patient factors

previous pregnancies, previous transfusions

 

Immune factors

Antibodies

HLA, platelet specific, erythrocyte

 

 

Others

 

Length of time the platelets are stored

 

Perform physical examination to look for:

Evidence of bleeding in skin, mucous membrane, joints, soft tissue

Lymphadenopathy

Splenomegaly

Step 4: Transfuse platelets (Table 62.6)

Three types of platelet products are commonly used in clinical practice:

– Random-donor platelets (RDP)

Table 62.7 Approach for management of thrombocytopenia

 

 

Etiology

Mechanism

Presentation

Treatment

ITP, after viral illness, may be

IgG antibodies against platelet antigens, platelet

All ages, common in young adult females

Steroids, prednisolone 1 mg/kg/day

associated with antiphospho

clearance by spleen, inadequate platelet

 

for 1–2 weeks, taper

lipid antibody syndrome, may

production response

Severe thrombocytopenia with normal

IVIG infusion 1g/kg/day for 2 days

be initial presentation of

 

RBC and WBC morphology and number

 

connective tissue disease,

 

Diagnosis by exclusion

Anti RhD antibodies 50–75 m/kg IV

lymphoploriferative malignancy

 

 

 

(Rh + Ve patients with intact spleen)

 

 

 

TTP-HUS

-Inherited or acquired deficiency of von

Microangiopathic hemolytic anemia,

FFP transfusions until the patient is

 

Willebrand factor cleaving protease

thrombocytopenia, renal insufficiency,

ready for plasma exchanges

 

(ADAMTS13)

fever, and mental status changes

 

 

Idiopathic or secondary to Escherichia coli

Schistiocytes in peripheral smear, raised

Plasma exchanges

 

diarrhea, HIV infection, certain drugs

LDH, normal coagulation profile

Platelet transfusions only in

 

(ticlopidine, clopidogrel, quinine, cyclosporine

 

life-threatening bleeding

 

A, mitomycin A, cisplatin, etc.), pregnancy, bone

 

 

 

marrow transplant, and metastatic carcinomas

 

 

Drug-induced thrombocytopenia

Antiplatelet agents’ and other drugs’ immune

History—no other blood or coagulation

Stop the offending drug

 

mechanism

abnormalities

Supportive care

 

Chemotherapy and alcohol—directly inhibit

Most chemotherapeutic drugs—nadir of

Supportive care

 

megakaryocytes

blood counts in 7–10 days, recovers over

 

 

 

2–3 weeks Nitrosureas and mitomycin

 

 

 

cause prolonged myelosuppression

 

 

Heparin—antibodies against heparin–platelet

Type I—modest transient thrombocytopenia

Spontaneous recovery

 

factor 4 complex

in 2–3 days after heparin therapy

 

 

 

Type II—less common, occurs 4–14 days

Stop heparin

 

 

after heparin therapy

 

 

 

ELISA assay for anti-PF 4 antibody,

Doppler to rule out thrombosis

 

 

serotonin release assay, platelet aggregation

Use direct thrombin inhibitors

 

 

studies

(argatroban, lepirudin) Fondaparinux

 

 

 

should be used with caution

 

 

 

LMWH and UFH should not be used

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