This is refractory shock with hypoxemic respiratory failure

1. Immediate priorities: do these now

A. Call for help and activate definitive-care pathways

• ICU consultant, anaesthesia/airway team, surgeon, cardiology/echo, and interventional radiology or cardiothoracic surgery.
• Activate a local PE response team or equivalent if available.
• Inform the operating surgeon immediately because major surgery 6 days ago substantially affects anticoagulation and thrombolysis decisions.
• Prepare for cardiac arrest. Apply defibrillator pads and have a resuscitation trolley at bedside.

B. Stop the possible trigger

• Stop albumin immediately.
• Do not restart it.
• Keep the albumin bottle, administration set, and records for reaction investigation.
• Check everything administered in the preceding hours: antibiotics, analgesics, antiemetics, contrast, blood products, heparin, chlorhexidine exposure, latex, line flushes.

C. Monitoring and access

• Arterial line urgently, if not already present.
• Two large-bore peripheral IV lines or reliable central access.
• Continuous ECG, SpO2, end-tidal CO2 if possible, temperature, urine output hourly.
• Send urgent bloods without delaying treatment:
  • ABG with lactate, repeated serially
  • CBC, platelet count
  • Electrolytes including ionized calcium and magnesium
  • Renal and liver function
  • Glucose
  • PT/INR, aPTT, fibrinogen, D-dimer only if diagnostically useful
  • Troponin, BNP or NT-proBNP
  • Group and crossmatch, blood bank alert
  • Blood cultures if sepsis is plausible, but do not delay antibiotics
  • Serum tryptase now or as close to 1-2 hours after onset as possible, and a baseline sample after recovery or at least 24 hours later if anaphylaxis is suspected.

D. Targets

• Aim initially for MAP at least 65 mmHg, while judging organ perfusion, urine output, capillary refill, mentation, and lactate trend.
• Give oxygen to correct hypoxaemia. If she is tiring, obtunded, cannot protect the airway, or oxygenation is failing, intubation may be needed, but it is high risk in massive PE or severe right-ventricular failure.

2. Most likely causes, in priority order

1. High-risk pulmonary embolism: most likely and must be excluded urgently

Why this fits

• Active malignancy, especially ovarian cancer
• Major pelvic oncologic surgery
• Postoperative day 6, a high-risk period for VTE
• Likely reduced mobility
• Previous chemotherapy and radiotherapy
• Sudden onset of hypoxaemia and shock

Why the ABG fits

• PaO2 70 mmHg on 10 L oxygen is concerning for major V/Q mismatch, shunt, low cardiac output, or pulmonary pathology.
• Base deficit -13 to -14 indicates a large metabolic acid burden, usually lactic acidosis from inadequate tissue perfusion in this setting.
• A “normal” pH does not reassure. It can represent mixed metabolic acidosis plus respiratory alkalosis from tachypnoea, pain, hypoxaemia, early sepsis, or PE. Review PaCO2, bicarbonate, lactate, and anion gap, not pH alone.

Key bedside findings

• Tachycardia, raised JVP, cool peripheries, oliguria, syncope
• ECG: sinus tachycardia, new RBBB, right heart strain pattern, though none are diagnostic
• Echo: dilated RV, poor RV function, septal flattening or D-shaped LV, small underfilled LV, elevated pulmonary pressures, sometimes thrombus in transit
• Leg compression ultrasound may show proximal DVT.

2. Anaphylaxis to albumin or another recent exposure

Why it remains highly important

• Hypotension began after albumin infusion.
• Severe anaphylaxis can be predominantly cardiovascular, with little or no rash, urticaria, bronchospasm, or facial swelling.
• It can cause severe distributive shock and capillary leak.
• Hypoxaemia can result from bronchospasm, upper-airway oedema, pulmonary oedema, or reduced cardiac output.

Features that would support it

• Onset during or soon after albumin exposure
• Urticaria, flushing, itching, angioedema
• Wheeze, increased airway pressure, stridor, bronchospasm
• Rapid vasodilatory shock with warm extremities early
• GI symptoms, though sedated or critically ill patients may not report these
• Raised acute serum tryptase, though a normal tryptase does not exclude anaphylaxis.

Important management implication

3. Hemorrhagic shock: concealed postoperative bleeding

Why it fits

• Intra-abdominal or retroperitoneal bleeding
• Pelvic hematoma
• Anastomotic or vaginal vault bleeding
• Bleeding potentiated by anticoagulants, thrombocytopenia, chemotherapy effects, or coagulopathy
• GI bleeding

Assess immediately

• Examine drains, wound, vaginal loss, abdomen, flank bruising
• Trending Hb is useful but may initially be falsely normal
• POCUS/FAST for free fluid, recognizing retroperitoneal bleeding may be missed
• Bedside abdominal ultrasound or urgent CT abdomen/pelvis only if stable enough
• Crossmatch and prepare blood products
• Check coagulation, fibrinogen, platelets, calcium, and temperature.

4. Septic shock, possibly abdominal/pelvic source

Why it fits

• Pelvic abscess
• Anastomotic leak or bowel injury
• Infected collection
• Catheter-associated infection
• Pneumonia
• Urinary sepsis
• Neutropenic or immunocompromised infection after chemotherapy

What to do

• Obtain blood cultures and cultures from likely sources promptly, but do not delay antibiotics in shock.
• Give broad-spectrum IV antibiotics according to local postoperative intra-abdominal sepsis guidance, after discussing with the surgical and microbiology teams.
• Search for source with focused abdominal/pelvic examination, bedside ultrasound, chest imaging, urine testing and CT when safely possible.
• If there is a collection, leak, necrotic tissue, or infected line, definitive source control is required.

5. Cardiogenic shock

• Acute coronary syndrome, including demand-mediated ischaemia
• Stress cardiomyopathy
• Chemotherapy-related cardiomyopathy
• Severe arrhythmia
• Acute myocarditis
• RV infarction
• Acute valvular event, less likely but possible

Tests

• 12-lead ECG now and serially
• Troponin and repeat testing
• Immediate focused echo: LV function, RV function, regional wall motion, valvular function, pericardial effusion
• Consider formal echo and cardiology review.

6. Tension pneumothorax, tamponade, or another obstructive process

Tension pneumothorax

• Unilateral absent breath sounds
• Marked asymmetry in chest expansion
• Sudden increased airway pressures if ventilated
• Absent lung sliding on ultrasound
• Hypotension and hypoxaemia

Cardiac tamponade

• Pericardial effusion, right-sided chamber collapse, plethoric IVC on POCUS
• Elevated JVP, pulsus paradoxus, tachycardia, hypotension

Air embolism

7. Acute lung pathology or transfusion-related complication

• Aspiration
• Atelectasis/mucus plugging
• Pulmonary oedema from cardiac failure or excessive fluids
• Pneumonia
• ARDS from sepsis
• TRALI/TACO if recent blood component exposure
• Pleural effusion

• B-lines and pleural effusions suggest oedema
• Consolidation suggests pneumonia/aspiration
• Absent lung sliding suggests pneumothorax
• A very small IVC may support hypovolaemia, but interpret in the context of ventilation and RV function.

3. Bedside diagnostic sequence: first 10-20 minutes

Immediate POCUS should answer five questions

1. Is the RV acutely failing?

• RV dilatation, often RV:LV ratio greater than 1
• Septal flattening, D-shaped LV
• Underfilled hyperdynamic LV
• Reduced RV systolic function
• Dilated IVC with poor collapse
• Occasionally clot in right heart or proximal pulmonary artery

2. Is there tamponade?

• Pericardial collection
• Right atrial or right ventricular diastolic collapse
• Plethoric IVC

3. Is there tension pneumothorax?

• No lung sliding and absent B-lines on affected side
• Lung point, if stable enough to identify

4. Is the LV failing?

• Poor global LV contractility or a regional wall-motion abnormality suggests cardiogenic shock/ACS.

5. Is there a proximal DVT?

• Bilateral common femoral and popliteal compression ultrasound.
• A new proximal DVT in this scenario strongly supports PE.

• Portable chest X-ray
• ECG
• Repeat ABG plus lactate
• Formal echocardiography as soon as possible
• CT pulmonary angiography only after she is stable enough for transfer, unless a different diagnosis is more likely and imaging will immediately change management.

4. Haemodynamic management

Fluids: cautious, reassessed boluses only

• In massive PE/RV failure, excess fluid distends the RV, worsens septal shift, and further reduces LV filling.
• In cardiogenic shock or pulmonary oedema, excess fluid worsens gas exchange.
• In hemorrhage, blood rather than repeated crystalloid is required.
• In anaphylaxis or vasodilatory sepsis, fluid requirements can be high, but should still be reassessed frequently.

Vasopressors/inotropes

• Noradrenaline is generally the initial vasopressor for persistent hypotension in distributive shock and is often useful in PE-related hypotension because it restores coronary perfusion pressure to the failing RV.
• In suspected massive PE with low cardiac output and RV failure, dobutamine may help contractility only after or alongside adequate vasopressor support. It can worsen hypotension if used without vasopressor cover.
• Adrenaline may be appropriate in refractory anaphylaxis or profound shock, but monitor for tachyarrhythmia, hyperlactataemia, myocardial ischaemia, and worsening acidosis.
• If vasoplegia persists despite escalating noradrenaline, many ICU protocols add vasopressin, but use local ICU policy and consultant oversight.

Correct contributors to catecholamine resistance

• Severe acidaemia reduces the response to catecholamines.
• Correct hypoxaemia.
• Treat hypocalcaemia, especially if large-volume transfusion is occurring.
• Correct severe hyperkalaemia or hypoglycaemia if present.
• Maintain normothermia.
• Avoid sedative-induced vasodilation wherever possible.

5. Management if massive PE is suspected or demonstrated

Immediate supportive strategy

• Oxygen, judicious ventilation, vasopressor support
• Avoid unnecessary intubation and excessive PEEP
• Avoid large fluid loading if echo shows RV strain
• Consider inhaled pulmonary vasodilator, such as inhaled nitric oxide or inhaled epoprostenol, as a rescue bridge in severe RV failure if available. This is not definitive treatment.

Anticoagulation

• It can be rapidly stopped
• It can be reversed with protamine
• It is preferred if catheter intervention, embolectomy, or thrombolysis may be required.

Reperfusion: the critical decision

Preferred options if available

1. Catheter-directed mechanical thrombectomy, with or without low-dose local thrombolytic therapy.
2. Surgical pulmonary embolectomy, especially if thrombolysis is contraindicated or failed.
3. VA-ECMO as a bridge in refractory circulatory collapse or cardiac arrest, where an experienced ECMO/PE center is available, combined with definitive reperfusion treatment.

6. Management if anaphylaxis is suspected

1. Stop albumin and any possible culprit infusion.
2. Call senior anaesthesia/ICU assistance.
3. Secure airway and give high-flow oxygen.
4. Place patient flat with legs elevated if tolerated. Avoid sitting upright in severe anaphylaxis because it can worsen venous return.
5. Give rapid IV crystalloid boluses, reassessing frequently. Anaphylaxis produces large intravascular fluid shifts.
6. Adrenaline is first line.
   • In a patient with profound shock already in ICU with arterial monitoring, a titrated IV adrenaline infusion by an experienced critical-care clinician is appropriate for refractory anaphylactic shock.
   • Avoid casual IV bolus adrenaline because dosing errors and arrhythmias are dangerous.
7. Nebulized salbutamol for persistent bronchospasm.
8. Antihistamines can improve skin symptoms but do not reverse airway obstruction or shock.
9. Corticosteroids are not emergency lifesaving therapy and should never delay adrenaline, fluids, airway management, or vasopressors.
10. Obtain acute tryptase, document all suspected exposures, and arrange allergy referral after recovery.

7. Acid-base interpretation and treatment

What the base deficit means

• Metabolic acidosis decreases bicarbonate and lowers pH.
• Compensatory hyperventilation lowers PaCO2 and raises pH.
• The final pH can look “normal,” despite severe physiological derangement.

Obtain and trend

• Lactate every 2-4 hours or more frequently during resuscitation
• PaCO2, HCO3-, anion gap, chloride, ketones if relevant
• Renal function and urine output
• Corrected ionized calcium
• Serial haemoglobin and coagulation profile.

Do not treat the number alone

• Relieving obstruction in PE/tamponade/tension pneumothorax
• Treating hemorrhage
• Treating anaphylaxis
• Restoring perfusion in sepsis/cardiogenic shock
• Optimizing oxygenation and haemoglobin.

8. A practical working plan for this exact case

Treat as “massive PE versus refractory anaphylactic shock,” while ruling out hemorrhage, tamponade, pneumothorax, cardiogenic shock, and sepsis.

1. Stop albumin now.
2. Senior ICU/anaesthesia/surgery/cardiology/IR involvement now.
3. Arterial line, repeated ABG/lactate, crossmatch, full shock blood panel, ECG, portable chest X-ray.
4. Immediate POCUS:
   • RV strain/underfilled LV?
   • Pericardial tamponade?
   • Pneumothorax?
   • LV failure?
   • DVT?
5. If RV strain plus shock or proximal DVT: manage as high-risk PE and urgently convene PE/reperfusion decision-makers.
6. If anaphylaxis remains plausible: continue carefully titrated adrenaline strategy, fluids guided by reassessment, bronchodilator if bronchospasm, collect tryptase.
7. Examine for bleeding and trend Hb/coagulation. If bleeding possible, prepare blood and obtain surgical assessment before full-dose anticoagulation or thrombolysis.
8. If no hemorrhagic contraindication and PE probability is high: discuss immediate IV UFH and definitive reperfusion strategy.
9. If unstable enough that CTPA is unsafe: do not delay life-saving decisions for CT. Use echo, DVT ultrasound, clinical probability, and multidisciplinary judgment.
10. Start broad-spectrum antibiotics if sepsis cannot be reasonably excluded after cultures are obtained, especially if lactate rises, fever/hypothermia, leukocyte abnormality, abdominal findings, or unexplained vasoplegia are present.
11. Escalate rapidly to catheter thrombectomy, surgical embolectomy, or ECMO-capable centre if shock persists.

Bottom line