GCC Nurse Guide: Coagulation Disorders & DIC

The Coagulation Cascade — Simplified

        Two pathways converge at Factor X to form a common pathway leading to fibrin clot
        Think of coagulation as a waterfall — each factor activates the next. The cascade amplifies a small signal into a large, stable clot.
      

Intrinsic Pathway (PTT/APTT)

Contact ActivationXII → XI → IX

↓

Factor VIII ComplexIXa + VIIIa activate X

Measured by: APTT (normal 25–35 sec)

Extrinsic Pathway (PT/INR)

Tissue Factor (TF)Released from damaged tissue

↓

TF + Factor VIIVIIa + TF activate X

Measured by: PT (normal 11–14 sec) / INR

Common Pathway

Factor Xa + Va (Prothrombinase Complex)Converts Prothrombin (II) → Thrombin (IIa)

↓

Thrombin (IIa)Converts Fibrinogen → Fibrin monomer → cross-linked clot (Factor XIII)

Primary vs Secondary Haemostasis

        Primary Haemostasis — Platelet Plug
        Vasoconstriction: Immediate response to vessel injury
Platelet adhesion: vWF bridges exposed collagen to platelet GPIb receptor
Platelet activation: ADP, thromboxane A2 released — shape change
Platelet aggregation: GPIIb/IIIa binds fibrinogen, forming platelet plug

      

        Secondary Haemostasis — Fibrin Clot
        Coagulation cascade activated on platelet surface
Thrombin converts fibrinogen to fibrin strands
Factor XIII cross-links fibrin — stable, insoluble clot
Plasmin (fibrinolysis) eventually dissolves clot — D-dimers released

      

        Clinical Memory Aid
        Primary (Platelet) = Platelet count & bleeding time — mucosal bleeding, petechiae

        Secondary (Clotting factors) = PT/APTT — deep bleeds, haemarthrosis, haematoma
      

Key Coagulation Lab Tests — Normal Values & Clinical Significance

Test	Normal Range	What It Measures	Clinical Significance
PT (Prothrombin Time)	11–14 seconds	Extrinsic + common pathway (Factors VII, X, V, II, I)	Prolonged in warfarin use, liver disease, DIC, Vit K deficiency
INR	0.9–1.2 (normal) 2.0–3.0 (therapeutic AF/VTE) 2.5–3.5 (mechanical valve)	Standardised PT ratio across labs	Therapeutic target depends on indication; >5 = high bleeding risk
APTT (Activated PTT)	25–35 seconds (ratio <1.5)	Intrinsic + common pathway (XII, XI, IX, VIII, X, V, II, I)	Prolonged in heparin therapy, haemophilia, DIC, lupus anticoagulant
Fibrinogen	2–4 g/L	Substrate for fibrin clot; acute phase reactant	<1.5 g/L = concern; <1.0 g/L = critical — give cryoprecipitate
D-dimer	<0.5 mg/L (FEU)	Fibrin degradation product — marker of active clot lysis	Elevated in DIC, PE, DVT, sepsis; high sensitivity, low specificity
Platelet Count	150–400 ×10&sup9;/L	Number of platelets available for primary haemostasis	<100 = thrombocytopenia; <50 = significant bleeding risk; <20 = spontaneous bleeding
Thrombin Time (TT)	14–19 seconds	Fibrinogen to fibrin conversion step only	Prolonged with heparin contamination, low fibrinogen, fibrinogen dysfunction

Anticoagulant Drugs & Their Targets

Drug Class	Examples	Target	Monitoring
Vitamin K Antagonist	Warfarin	Inhibits Vit K-dependent factors II, VII, IX, X; Protein C & S	INR (PT-based)
Unfractionated Heparin	UFH IV/SC	Potentiates antithrombin III — inhibits thrombin (IIa) & Xa	APTT (ratio 1.5–2.5)
LMWH	Enoxaparin, Dalteparin	Primarily anti-Xa activity	Anti-Xa level (renal impairment)
Direct Xa inhibitors	Rivaroxaban, Apixaban	Directly inhibit Factor Xa	Anti-Xa DOAC assay (not routine)
Direct Thrombin inhibitor	Dabigatran, Argatroban	Directly inhibit Thrombin (IIa)	ECT or diluted TT (not routine)
Fondaparinux	Fondaparinux	Indirect Xa inhibitor (via AT III)	Anti-Xa level

Viscoelastic Testing: TEG & ROTEM

        Point-of-care clot assessment — primarily used in ICU, cardiac surgery, trauma, obstetrics
        Unlike conventional tests (PT/APTT), TEG and ROTEM assess the entire clotting process in whole blood, including fibrinolysis.
      

Parameter	What It Reflects	Abnormality
R time (TEG) / CT (ROTEM)	Time to initial clot formation (clotting factors)	Prolonged = factor deficiency / heparin effect
K time / CFT	Clot kinetics — how fast clot strengthens	Prolonged = low fibrinogen or platelet dysfunction
Alpha angle (α)	Rate of fibrin and platelet cross-linking	Decreased = low fibrinogen
MA / MCF	Maximum clot strength (platelets + fibrin)	Reduced = thrombocytopenia or platelet dysfunction
LY30 / LI30	Clot lysis at 30 min (fibrinolysis)	Elevated = hyperfibrinolysis (major haemorrhage, DIC)

Guides targeted blood product use Reduces unnecessary FFP/platelet use Available in major GCC trauma centres

What is DIC? — The Paradoxical Coagulopathy

      DIC = Simultaneous pathological clotting AND bleeding — the patient clots and bleeds at the same time
      Disseminated Intravascular Coagulation is NOT a disease — it is a syndrome triggered by an underlying condition that causes widespread activation of the coagulation system, consuming clotting factors and platelets, leading to both microvascular thrombosis and haemorrhage.
    

CLOT

Microthrombi in vessels

Organ ischaemia: kidneys, lungs, brain, skin (purpura fulminans)

CONSUME

Factor & platelet consumption

Fibrinogen, Factors V, VIII, platelets rapidly depleted

BLEED

Haemorrhage from multiple sites

IV sites, surgical wounds, mucosa, brain, GI tract

Causes of DIC — STOP THE BLEED Mnemonic

Sepsis — most common cause; gram-negative endotoxins most potent; gram-positive also implicated

Trauma — massive tissue damage; head injury (high TF brain tissue)

Obstetric — abruption, amniotic fluid embolism (AFE), PPH, retained products, pre-eclampsia/HELLP

Post-transfusion reaction — acute haemolytic reaction triggers DIC

Tumour / Malignancy — APL (AML-M3) classically; mucin-secreting adenocarcinomas

Hepatic failure — reduces clearance of activated factors

Envenomation — snake bite (viper venom contains procoagulant enzymes)

Burns — extensive burns release tissue factor and inflammatory mediators

Low temperature — hypothermia (part of lethal triad with acidosis)

Extra-vascular haemolysis — ABO incompatible transfusion

Drugs / toxic — MDMA, cocaine, some chemotherapy agents

ISTH Overt DIC Scoring System

        Score ≥5 = Compatible with Overt DIC — treat aggressively
        Score <5 = Non-overt (subclinical) DIC — repeat scoring daily; treat underlying cause
      

Parameter	Result	Score
Platelet Count	>100 ×10&sup9;/L	0
	50–100 ×10&sup9;/L	1
	<50 ×10&sup9;/L	2
PT Prolongation	<3 seconds above normal	0
	3–6 seconds above normal	1
	>6 seconds above normal	2
Fibrinogen	>1 g/L	0
Fibrinogen	<1 g/L	1
D-dimer / Fibrin Degradation Products	No increase	0
	Moderate increase	2
	Strong increase	3

        Maximum score = 8 | Score ≥5 = Overt DIC | Repeat daily if score 3–4
        Requires a predisposing condition — only score if underlying diagnosis known.
      

Clinical Presentation of DIC

Look for bleeding from multiple sites simultaneously — a classic red flag

Oozing from IV cannula sites — often the first nursing observation
Petechiae and purpura — platelet consumption; skin mottling
Purpura fulminans — skin necrosis from microvascular thrombosis; classic in meningococcal sepsis
Mucosal bleeding — gums, epistaxis, GI bleeding (PR / melaena)
Haematuria — renal microthrombi / bleeding
Haemoptysis / pulmonary haemorrhage — severe DIC
Intracranial haemorrhage — rare but catastrophic
Organ dysfunction signs — oliguria (renal), confusion (cerebral), jaundice (hepatic)
Wound haemorrhage — operative sites bleed relentlessly

DIC Lab Pattern — What to Expect

Test	DIC Finding	Significance
Platelet count	↓ Falling / Low	Platelets consumed in microthrombi
PT / INR	↑ Prolonged	Clotting factors consumed
APTT	↑ Prolonged	Factors V, VIII, X consumed
Fibrinogen	↓ Low (<1.5 g/L)	Consumed in clot formation; proteolysed by plasmin
D-dimer / FDP	↑↑ Markedly elevated	Massive fibrin breakdown occurring
Blood film	Schistocytes (fragmented RBCs)	Microangiopathic haemolytic anaemia (MAHA)
Haemoglobin	↓ Low	Haemolysis + haemorrhage
LDH	↑ Elevated	Red cell destruction; organ ischaemia

        Microangiopathic Haemolytic Anaemia (MAHA)
        Schistocytes (fragmented red cells) seen on blood film — red cells literally shredded by fibrin strands in micro-vessels. Also occurs in TTP, HUS, HELLP syndrome.
      

Priority #1 — Treat the Underlying Cause

      Blood products buy time — they do NOT cure DIC. The only cure is removing the trigger.
      DIC will continue to consume blood products until the underlying cause is treated.
    

1
Identify and treat the trigger: sepsis = broad-spectrum antibiotics + source control; obstetric = deliver baby/placenta; trauma = haemostatic surgery
2
Resuscitate: restore perfusion pressure — without adequate cardiac output, all treatments fail
3
Correct physiological derangements: temperature (warm to >36°C), pH (target pH >7.35), ionised calcium (Ca²+ >1.1 mmol/L)
4
Replace consumed factors: guided by lab results and clinical bleeding (see blood products below)
5
Recheck coagulation: repeat FBC, PT/APTT, fibrinogen, D-dimer every 4–6 hrs during active DIC

FFP — Fresh Frozen Plasma

Replaces ALL clotting factors in physiological proportions

Parameter	Detail
Volume	~200–300 mL per unit
Dose in DIC	15 mL/kg (typically 4–6 units in an adult)
Indication	Prolonged PT/APTT (>1.5× normal) with active bleeding
Infusion rate	As fast as patient tolerates; 30–60 min per unit
ABO compatibility	ABO compatible required; Rh not required
Storage after thaw	Use within 4 hrs (24 hrs at 1–6°C)

NOT for volume replacement alone Volume overload risk — monitor for TACO

Cryoprecipitate — Concentrated Fibrinogen

        Give when fibrinogen <1.5 g/L with active bleeding — target >2 g/L in massive haemorrhage
      

Parameter	Detail
Contents	Fibrinogen, Factor VIII, vWF, Factor XIII, Fibronectin
Volume	10–20 mL per unit; given as pool of 5–10 units (~150–200 mL)
Dose	10 units (pool) — raises fibrinogen by ~1 g/L in adult
Indication	Fibrinogen <1.5 g/L with bleeding; <1 g/L always give
Use within	4 hrs once thawed
Alternative	Fibrinogen concentrate (RiaSTAP) — available in some GCC centres

Key in obstetric haemorrhage (PPH) Prioritise over FFP when fibrinogen low

Platelets in DIC

Threshold	Action
<50 ×10&sup9;/L + active bleeding	Transfuse platelets — aim >50 ×10&sup9;/L
<20 ×10&sup9;/L (no active bleed)	Prophylactic transfusion to prevent spontaneous haemorrhage
<100 ×10&sup9;/L + neurosurgery/neurotoxic risk	Transfuse to maintain >100 ×10&sup9;/L
50–100 ×10&sup9;/L — procedures	Transfuse pre-procedure

        Platelets consumed rapidly in active DIC
        Recheck platelet count 1 hour post-transfusion to assess increment. Poor increment suggests ongoing consumption or alloimmunisation.
      

Red Blood Cells & Calcium

        Red Blood Cells (PRBC)
        Transfuse if Hb <80 g/L in actively bleeding patient
Restrictive threshold (Hb <70 g/L) for non-bleeding, haemodynamically stable patient
In massive haemorrhage: give within MTP 1:1:1 ratio

      

        Ionised Calcium — Critical in Massive Transfusion
        Blood products contain citrate as anticoagulant — chelates calcium
Hypocalcaemia impairs platelet function and coagulation
Calcium gluconate 10 mL 10% IV for every 4 units transfused (or per ionised Ca²⁺)
Calcium chloride preferred in cardiac arrest / haemodynamic compromise

      

Massive Transfusion Protocol (MTP) — 1:1:1

        MTP activation: >10 units PRBC in 24 hrs, or anticipated massive haemorrhage
        Early activation prevents dilutional coagulopathy and the lethal triad.
      

RBC (Packed Red Cells)

Oxygen-carrying capacity

FFP (Fresh Frozen Plasma)

All clotting factors

Platelets

Primary haemostasis

Fibrinogen EARLY: give cryoprecipitate or fibrinogen concentrate early in MTP — do not wait for fibrinogen to fall critically
Calcium gluconate with each MTP pack
Use blood warmer — hypothermia worsens coagulopathy
Monitor temperature, pH, ionised calcium throughout
Communicate with blood bank — give early warning

Tranexamic Acid (TXA) & Heparin in DIC

        Tranexamic Acid — Antifibrinolytic
        Mechanism: inhibits plasmin (blocks fibrinolysis) — preserves clot
CRASH-2 trial: 1g IV over 10 min within 3 hrs of trauma, then 1g over 8 hrs
Obstetric: given in PPH (1g IV; repeat if bleeding continues after 30 min)
AVOID in DIC with predominant thrombosis — may worsen organ ischaemia
Use in hyperfibrinolytic DIC (post-trauma, obstetric) with CAUTION

      

        Heparin in DIC — Highly Controversial
        Generally AVOIDED in DIC with haemorrhage — worsens bleeding
Consider ONLY if thrombosis predominates: purpura fulminans, acral ischaemia, extensive deep vein thrombosis
Low-dose UFH infusion may be used in specialist haematology consultation
Chronic DIC (e.g., Trousseau syndrome in malignancy) — LMWH may be appropriate

      

ISTH DIC Probability Scorer

Interactive ISTH overt DIC scoring — requires a predisposing condition to be valid

Platelet Count

PT Prolongation (above normal)

Fibrinogen Level

D-dimer / Fibrin Degradation Products

Haemophilia A & B — Inherited Factor Deficiencies

Feature	Haemophilia A	Haemophilia B
Deficient Factor	Factor VIII	Factor IX ("Christmas disease")
Inheritance	X-linked recessive	X-linked recessive
Lab finding	Prolonged APTT; PT normal	Prolonged APTT; PT normal
Treatment	Factor VIII concentrate (recombinant preferred)	Factor IX concentrate
Mild (5–40%)	DDAVP (desmopressin) — releases stored FVIII	Factor IX concentrate
Inhibitors	Bypassing agents: rFVIIa (NovoSeven), FEIBA	As per Haemophilia A
Prophylaxis	Regular factor infusions 3×/week	1–2×/week infusions

        Nursing: haemophilia bleeds
        Target joint (haemarthrosis): immobilise, ice, elevate — give factor concentrate FIRST, then analgesic
NEVER give IM injections — use SC or IV only
Avoid NSAIDs — use paracetamol for pain
Ensure Medical Alert wearable documented; factor product card carried by patient
GCC: Saudi Arabia has national haemophilia centre (NBAD); UAE, Qatar have dedicated haematology programmes

      

Von Willebrand Disease (vWD)

        Most common inherited bleeding disorder worldwide — affects ~1% of population
        vWF (von Willebrand Factor) bridges platelet GPIb to exposed collagen AND carries Factor VIII in plasma.
      

Type	Defect	Lab	Treatment
Type 1 (most common ~75%)	Quantitative — low vWF levels	↑ APTT (mild), ↓ vWF antigen	DDAVP (desmopressin) — releases endothelial vWF stores
Type 2 (qualitative variants)	Qualitative — vWF dysfunction	Variable; vWF activity low	vWF concentrate (Humate-P); DDAVP may be contraindicated in 2B
Type 3 (severe, rare)	Complete absence of vWF	Markedly ↓ vWF; very ↑ APTT	vWF/FVIII concentrate always; DDAVP ineffective

        DDAVP (Desmopressin) — mechanism
        Causes release of pre-formed vWF from Weibel-Palade bodies in endothelial cells. Effective for Type 1 vWD and mild Haemophilia A. Dose: 0.3 mcg/kg IV over 30 min or intranasal. Risk: hyponatraemia — monitor Na⁺; fluid restrict for 24 hrs.
      

HIT — Heparin-Induced Thrombocytopenia

        CRITICAL: Paradoxical thrombocytopenia that causes life-threatening THROMBOSIS — not bleeding
        HIT antibodies (anti-PF4/heparin IgG) activate platelets, causing thrombosis while platelet count falls.
      

4T Score — Pre-test probability

T	2 points	1 point	0 points
Thrombocytopenia	>50% fall; nadir ≥20	30–50% fall; nadir 10–19	<30% fall; nadir <10
Timing	Days 5–10, or <1 day if prior heparin	Beyond day 10; unclear	≤4 days (no prior heparin)
Thrombosis	New thrombosis; skin necrosis	Progressive/recurrent thrombosis	None
oTher causes	No other cause	Possible other cause	Definite other cause

Score 0–3 = Low probability | 4–5 = Intermediate | 6–8 = High probability

        HIT Management — Act Immediately
        STOP ALL heparin immediately — including heparin flushes, LMWH, heparin-coated catheters
Do NOT transfuse platelets (unless life-threatening haemorrhage)
Start non-heparin anticoagulant: Argatroban (IV; liver metabolism) or Fondaparinux (SC; preferred if renal function adequate)
Test for HIT antibodies (anti-PF4 ELISA)
Transition to warfarin ONLY when platelets >150 ×10&sup9;/L — warfarin alone in acute HIT risks thrombosis
Document heparin allergy — lifelong heparin avoidance

      

Thrombocytopenia — Key Types

ITP — Immune Thrombocytopenic Purpura▼

Autoimmune — anti-platelet antibodies (anti-GPIIb/IIIa) destroy platelets in spleen
Diagnosis of exclusion; no splenomegaly; normal coagulation (PT/APTT normal)
First-line: prednisolone 1 mg/kg/day; IV immunoglobulin (IVIG) for rapid response needed
Second-line: rituximab, splenectomy, thrombopoietin receptor agonists (eltrombopag, romiplostim)
Transfuse platelets only if severe bleeding — platelets destroyed rapidly

TTP — Thrombotic Thrombocytopenic Purpura▼

ADAMTS13 deficiency (protease that cleaves ultra-large vWF multimers)
Classic pentad: MAHA + thrombocytopenia + neurological symptoms + fever + renal failure
PLASMIC score used for pre-test probability
Emergency: plasma exchange (PEX/TPE) + steroids + rituximab
DO NOT transfuse platelets — "pour fuel on fire" — risk of thrombosis
Caplacizumab (anti-vWF nanobody) — newer adjunct therapy

Drug-Induced Thrombocytopenia▼

Quinine, vancomycin, linezolid, valproate, chemotherapy agents most common
Stop the offending drug — platelet count typically recovers within 7–10 days
Review medication list carefully when new thrombocytopenia detected

Warfarin Reversal — Supratherapeutic INR

INR	Clinical Status	Action
4.5–10	No bleeding	Withhold 1–2 doses; oral Vitamin K 1–2 mg; recheck INR next day
>10	No bleeding	Withhold warfarin; oral Vitamin K 5 mg; recheck INR in 24 hrs
Any elevated	Minor bleeding	Withhold warfarin; oral/IV Vitamin K 1–3 mg; supportive care
Any elevated	Major / life-threatening bleeding	4-factor PCC (Beriplex/Octaplex) immediately + IV Vitamin K 10 mg; FFP if PCC unavailable
Any elevated	Intracranial haemorrhage	4-factor PCC + IV Vitamin K 10 mg; urgent neurosurgical review

        4-factor PCC (Prothrombin Complex Concentrate)
        Contains Factors II, VII, IX, X — faster and more reliable reversal than FFP. Small volume (20–30 mL vs 600–900 mL for FFP). INR reverses within 15–30 minutes. Risk of thrombosis — use only for major haemorrhage.
      

DOAC Reversal Agents

        Standard coag tests (PT/APTT) do not reliably measure DOAC effect — do not use to guide treatment
      

DOAC	Target	Specific Reversal Agent	Dose
Dabigatran	Thrombin IIa	Idarucizumab (Praxbind)	5g IV (2 × 2.5g boluses)
Rivaroxaban	Factor Xa	Andexanet alfa (Ondexxya)	Weight/dose-based; bolus + infusion
Apixaban	Factor Xa	Andexanet alfa (Ondexxya)	Weight/dose-based; bolus + infusion
Edoxaban	Factor Xa	Andexanet alfa (off-label) or 4-factor PCC	PCC 25–50 IU/kg if reversal agent unavailable

        Liver Disease Coagulopathy
        Both pro-coagulants (Factors II, VII, IX, X) AND anti-coagulants (Protein C, S, Antithrombin) are reduced. The coagulation system is rebalanced — standard PT/INR overestimates bleeding risk. TEG/ROTEM preferred to guide blood product use. Do not correct INR alone without clinical bleeding indication.
      

ABCDE Approach to Major Haemorrhage

A
Airway: maintain — massive aspiration risk in obtunded bleeding patient; consider early intubation if GCS ≤8
B
Breathing: high-flow oxygen 15 L/min via non-rebreather mask; assess for haemothorax or haemoptysis
C
Circulation: 2× large-bore IV access (14–16G); activate MTP; fluid resuscitation (permissive hypotension in trauma — target SBP 80–90 mmHg until haemostasis); blood products > crystalloid
D
Disability: GCS, AVPU; peripheral perfusion; signs of cerebral hypoperfusion
E
Exposure & Control: expose fully; identify all bleeding sites; direct pressure; wound packing; tourniquet; keep patient warm (reflective blanket)

Wound Packing & Haemostatic Dressings

        Direct pressure remains the single most effective first-line intervention for external haemorrhage
        Apply firm, continuous pressure for minimum 5–10 minutes. Do not lift to check — this dislodges the clot.
      

QuikClot Combat Gauze: kaolin-impregnated gauze — activates intrinsic pathway; preferred in military and trauma; pack firmly into wound cavity
Celox: chitosan-based — binds red cells and platelets independent of clotting cascade; effective in anticoagulated patients and hypothermia
HemCon bandage: chitosan-based; adheres to wound surface
Packing technique: tightly pack wound from base; apply pressure dressing on top; do not remove packing in pre-hospital setting
Wound packing most effective for junctional wounds (groin, axilla, neck) where tourniquet cannot be applied

Tourniquet Application

        Life over limb — tourniquet application is a nursing skill that saves lives
        Do not hesitate to apply a tourniquet when limb haemorrhage is not controlled by pressure alone.
      

1
Apply tourniquet 5–7 cm (2 inches) above the wound — never over a joint
2
Tighten until bleeding stops — this requires significant pressure; a tourniquet that doesn't stop bleeding is too loose
3
Write time of application on skin or tourniquet label — critical for surgical team
4
Do NOT remove the tourniquet in the field — only remove in controlled surgical environment
5
Safe duration: 2 hrs maximum; beyond 6 hrs = limb necrosis very likely — communicate urgently
6
Document: time applied, site, who applied, neurovascular status distal to tourniquet

CAT Tourniquet standard in GCC trauma SOFTT-W for junctional wounds

Trauma-Induced Coagulopathy (TIC) — The Lethal Triad

COLD

Hypothermia (<35°C)

Impairs enzyme activity; platelet dysfunction below 34°C; cardiac arrhythmias below 32°C

ACID

Acidosis (pH <7.35)

Impairs thrombin generation; thrombocytopenia worsened; all clotting enzyme reactions slowed

CLOT

Coagulopathy

Both cause and consequence of haemorrhage; each element worsens the others

        Breaking the lethal triad — Damage Control Resuscitation (DCR)
        Warm all IV fluids and blood products — blood warmers mandatory in major haemorrhage
Active patient warming: forced air warming blankets, warm environment
Correct acidosis: restore perfusion (not just bicarbonate); permissive hypotension
Minimise crystalloids: large volumes worsen dilutional coagulopathy and hypothermia
1:1:1 MTP ratio restores balanced haemostasis

      

Massive Transfusion Monitoring Complications

Complication	Cause	Nursing Action
Hypocalcaemia	Citrate in blood products chelates Ca²⁺	Calcium gluconate 10 mL 10% IV q4 units; monitor ionised Ca²⁺
Hypothermia	Cold blood products; heat loss from exposure/haemorrhage	Blood warmer; forced-air warming blanket; warm IV fluids
Hyperkalaemia	RBC lysis releases intracellular K⁺ (older stored blood)	12-lead ECG; continuous monitoring; glucose-insulin if severe; use freshest blood in neonates
TACO (Transfusion-associated circulatory overload)	Volume overload — especially FFP	Monitor fluid balance, SpO2, BP; IV furosemide; CXR
TRALI (Transfusion-related acute lung injury)	Anti-HLA antibodies in donor plasma	Stop transfusion; high-flow O2; often requires intubation; report to blood bank
Dilutional coagulopathy	Excessive crystalloid / PRBC without clotting factors	Adhere to 1:1:1 MTP; monitor PT/fibrinogen; give FFP and cryoprecipitate early

Obstetric Haemorrhage — PPH Management

        PPH: blood loss >500 mL vaginal delivery; >1000 mL caesarean section — Massive PPH: >2500 mL or shock
      

1
Call for help immediately: senior midwife, obstetrician, anaesthetist, blood bank — parallel response
2
4 T's assessment: Tone (uterine atony — most common, 80%), Tissue (retained products), Trauma (lacerations), Thrombin (coagulopathy)
3
Uterotonic drugs: oxytocin (first-line); ergometrine; carboprost (Hemabate); misoprostol — given per protocol
4
Uterine massage and bimanual compression
4
Tranexamic acid 1g IV: within 3 hrs of delivery onset; repeat if bleeding continues
5
Balloon tamponade: intrauterine balloon (Bakri balloon) — nursing: observe for re-bleeding, monitor vitals q15 min
6
B-Lynch suture, uterine artery ligation, hysterectomy — escalating surgical management; nursing prepares for theatre

        GCC Context — Obstetric Haemorrhage
        Higher parity rates in GCC populations increase PPH risk (uterine atony). Consanguinity-related inherited coagulopathies (Haemophilia A carriers, vWD) may complicate delivery. Pre-delivery coagulation screening important. Blood bank communication is critical — maintain open communication throughout.
      

Gastrointestinal Haemorrhage — Nursing Overview

Upper GI vs Lower GI — recognition and initial management

Feature	Upper GI Bleed	Lower GI Bleed
Presentation	Haematemesis, melaena, coffee-ground vomit	Haematochezia (fresh PR blood), dark melaena
Common causes	PUD, varices, Mallory-Weiss, oesophagitis	Diverticulosis, angiodysplasia, colorectal cancer, IBD, haemorrhoids
Scoring	Glasgow-Blatchford score (pre-endoscopy)	Oakland score (safe discharge)
Key nursing	NBM; NG tube if haematemesis; 2 large-bore IV; urgent endoscopy prep	Maintain IV access; stool charting; prompt colonoscopy coordination
Variceal bleed	Terlipressin or octreotide infusion; balloon tamponade (Sengstaken-Blakemore); antibiotics (norfloxacin/ceftriaxone)	—

Resuscitate before endoscopy if unstable Transfuse to Hb >70–80 g/L (target 70 in variceal) PPI infusion post-endoscopy for PUD

ISTH DIC Score — Quick Reference Table

Parameter	0 pts	1 pt	2 pts	3 pts
Platelets	>100	50–100	<50	—
PT prolongation	<3 sec	3–6 sec	>6 sec	—
Fibrinogen	>1 g/L	<1 g/L	—	—
D-dimer / FDP	Normal	—	Moderate ↑	Strong ↑
Score ≥5 = Overt DIC \| Score <5 = Non-overt (repeat daily)

Blood Product Quick Comparison

Product	Replaces / Contains	Trigger	Key Dose
PRBC	Red cells / Hb	Hb <70–80 g/L + bleeding	1 unit → +10 g/L Hb
FFP	ALL clotting factors (I–XII)	PT/APTT >1.5× + bleeding	15 mL/kg (~4–6 units)
Cryoprecipitate	Fibrinogen, FVIII, vWF, FXIII	Fibrinogen <1.5 g/L	10 units pool → ↑1 g/L
Platelets	Platelets for primary haemostasis	<50 + bleeding; <20 prophylaxis	1 dose → +30–50 ×10&sup9;/L
4-factor PCC	Factors II, VII, IX, X	Warfarin reversal + major bleed	25–50 IU/kg
Idarucizumab	Dabigatran reversal only	Dabigatran + life-threatening bleed	5g IV (2 × 2.5g)
Andexanet alfa	Reverses apixaban/rivaroxaban	Xa-inhibitor + life-threatening bleed	Dose-dependent protocol

HIT Recognition & Management Algorithm

          Step 1: Suspect HIT
          Platelet count falls >50% from baseline on days 5–10 of heparin therapy (or sooner if prior heparin exposure within 30–100 days)
        

          Step 2: Apply 4T Score
          Score 0–3 = Low (HIT unlikely); 4–5 = Intermediate; 6–8 = High probability
        

          Step 3: If 4T score ≥4 — STOP all heparin NOW
          Include UFH, LMWH, heparin flushes, heparin-coated catheters
        

          Step 4: Start alternative anticoagulation
          Argatroban (IV DTI) — preferred in renal failure (hepatic metabolism)
Fondaparinux (SC, anti-Xa) — preferred if renal function adequate
Danaparoid where available

        

          Step 5: Confirm with HIT antibody test
          Anti-PF4/heparin ELISA (functional assay: SRA most specific). Continue alternative anticoagulation regardless of test result if clinical suspicion high (4T ≥4).
        

          Step 6: Transition to long-term anticoagulation
          Warfarin ONLY when platelets >150 ×10&sup9;/L; overlap with alternative anticoagulant for ≥5 days. Document heparin allergy permanently.
        

DHA / DOH / SCFHS / QCHP High-Yield Exam Questions

Q: A patient on heparin infusion develops a 60% platelet drop on day 7. What is the priority nursing action?▼

Answer: Stop all heparin immediately and notify the doctor — suspect HIT.

Apply the 4T score. Do NOT wait for lab confirmation before stopping heparin if clinical suspicion is high. A non-heparin anticoagulant (argatroban or fondaparinux) should be started. Do NOT transfuse platelets. Document heparin allergy.

Q: What is the ISTH DIC score threshold for overt DIC?▼

Answer: Score ≥5 = Compatible with overt DIC. Score <5 = Non-overt; repeat daily.

Maximum score is 8. Parameters: platelet count (0–2), PT prolongation (0–2), fibrinogen (0–1), D-dimer (0–3). Requires a predisposing condition to be clinically valid.

Q: When should cryoprecipitate be given?▼

Answer: When fibrinogen <1.5 g/L with active bleeding; <1.0 g/L always give regardless.

In massive haemorrhage the target fibrinogen is >2 g/L. Cryoprecipitate contains fibrinogen, Factor VIII, vWF, Factor XIII, and fibronectin. A pool of 10 units raises fibrinogen by approximately 1 g/L in an adult. It is more fibrinogen-efficient than FFP.

Q: What is the reversal agent for dabigatran?▼

Answer: Idarucizumab (Praxbind) — 5g IV (given as two 2.5g boluses).

Idarucizumab is a humanised monoclonal antibody fragment that binds dabigatran with very high affinity (350× higher than thrombin). For apixaban and rivaroxaban (Factor Xa inhibitors), the reversal agent is andexanet alfa (Ondexxya). 4-factor PCC is an alternative when specific reversal agents are unavailable.

Q: What is the most common inherited bleeding disorder?▼

Answer: Von Willebrand Disease (vWD) — affects approximately 1% of the population.

vWD Type 1 is the most common subtype (75%). vWF bridges platelets to collagen (GPIb receptor) and carries Factor VIII in plasma. Treatment of Type 1: DDAVP (desmopressin) which releases stored vWF from endothelial cells. Monitor for hyponatraemia after DDAVP administration.

Q: A trauma patient has a pH of 7.28, temperature of 34°C, and bleeding from multiple wound sites. What is this called?▼

Answer: The Lethal Triad of trauma — hypothermia, acidosis, and coagulopathy.

Also known as Trauma-Induced Coagulopathy (TIC). Management: Damage Control Resuscitation — warm all blood products, use blood warmer, give 1:1:1 MTP, minimise cold crystalloids, correct acidosis by restoring perfusion, apply warming blankets. Breaking the triad is life-saving.

Q: What does a markedly elevated D-dimer with low fibrinogen and low platelets indicate?▼

Answer: Pattern consistent with Disseminated Intravascular Coagulation (DIC).

The classic DIC lab pattern: ↓ platelets (consumed in microthrombi), ↑ PT and APTT (clotting factors consumed), ↓ fibrinogen (consumed and degraded by plasmin), ↑↑ D-dimer (massive fibrin breakdown). Schistocytes on blood film = MAHA. ISTH score ≥5 = overt DIC. Treatment: treat the underlying cause first, then replace blood products.

Q: What is the MTP ratio for massive transfusion?▼

Answer: 1:1:1 — one unit of PRBC : one unit of FFP : one unit/dose of Platelets.

This ratio aims to replicate whole blood composition and prevent dilutional coagulopathy. Fibrinogen (cryoprecipitate) should be given early — do not wait for fibrinogen to fall below 1 g/L. Give calcium gluconate with each transfusion pack to counteract citrate-induced hypocalcaemia. Use blood warmer to prevent hypothermia.

Normal Coagulation Values — Quick Reference

0.9–1.2

INR (normal)

2–3 = therapeutic AF/VTE; 2.5–3.5 = mechanical valve

25–35 s

APTT

Ratio <1.5; therapeutic heparin = ratio 1.5–2.5

2–4 g/L

Fibrinogen

<1.5 = concern; <1.0 = critical — give cryoprecipitate

<0.5

D-dimer (mg/L)

High sensitivity; low specificity — always interpret with clinical context

150–400

Platelets (×10&sup9;/L)

<100 = thrombocytopenia; <50 = significant risk; <20 = spontaneous bleed

14–19 s

Thrombin Time

Prolonged: heparin, low fibrinogen, fibrinogen dysfunction

GCC Nursing Context — Coagulation-Specific Points

        Consanguinity & Inherited Coagulopathies
        Higher rates of consanguineous marriage in GCC populations increase prevalence of autosomal recessive conditions including Glanzmann's thrombasthenia (GPIIb/IIIa deficiency — platelet function disorder), Factor XIII deficiency, and severe vWD Type 3. Pre-marital and antenatal screening programmes are in place across all GCC states.
      

        Obstetric Haemorrhage Risk
        Higher gravidity (multiparity) in GCC populations increases PPH risk from uterine atony. Fibrinogen levels fall rapidly in obstetric DIC (AFE, abruption). Early cryoprecipitate in obstetric haemorrhage is evidence-based (OxOMM study). All delivery units should have pre-prepared PPH trolleys with cryoprecipitate protocols.
      

        Regulatory Exam Focus (SCFHS/DHA/QCHP/MOH)
        Commonly tested: ISTH DIC score thresholds; HIT management (stop heparin, argatroban/fondaparinux); DOAC reversal agents; warfarin reversal (PCC + Vitamin K); cryoprecipitate trigger (fibrinogen <1.5); MTP ratio (1:1:1); lethal triad of trauma; TTP (plasma exchange — do NOT give platelets); vWD most common inherited bleeding disorder.
      

        TEG/ROTEM Availability
        Viscoelastic testing increasingly available in major GCC hospitals (KFSH&RC, Cleveland Clinic Abu Dhabi, HMC Doha, Hamad Medical Corporation). Guides blood product use in cardiac surgery, liver transplant, major trauma. Nurses in ICU and cardiac theatres may interpret ROTEM traces — understanding MA/MCF, LY30 parameters important for exam.
      

Coagulation Disorders & DIC Nursing

ISTH DIC Probability Scorer