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ICU Fellowship Vivas – Submassive PE, Esophageal Perforation & Malaria

Dr Swapnil Pawar September 19, 2021 268 1

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    ICU Fellowship Vivas – Submassive PE, Esophageal Perforation & Malaria
    Dr Swapnil Pawar

Writtten by – Dr Madhuri Anupindi

1. You have been called to the gynaecology ward to review a 45-year-old female who is 48 hours post laparotomy for large bowel obstruction and is now tachypnoeic and hypotensive. BG of ovarian malignancy for which she has received chemotherapy. At surgery, she was found to have metastatic disease and has undergone a debulking procedure and bowel resection with the formation of a de-functioning ileostomy. Vital signs are GCS 15, RR 35, sats 90% on 8L via Hudson mask, few bibasal crepitations, HR 110, BP 80/40, soft distended abdomen with a pink functioning stoma. List your differential diagnoses for her presentation.

There are numerous potential causes for her presentation with my primary differentials being either a pulmonary embolism or hospital-acquired pneumonia. Other differentials include

  • Infection: other infections causing sepsis: intra-abdominal sepsis – less likely with the soft abdomen and functioning stoma
  • Inflammatory: aspiration, ischaemic bowel
  • Cardiac: ischaemia causing cardiac failure, exacerbation of chemotherapy-induced cardiomyopathy
  • Drug: allergic reaction, transfusion-related lung injury, pneumonitis secondary to chemotherapy
  • Secondary to malignancy: lymphangitis carcinomatosis (less likely – unlikely to cause rapid decline and hypotension unless causing pulmonary HTN and thus cardiac decompensation), diffuse alveolar haemorrhage
  • Trauma: less likely pneumothorax, a complication from OT such as perforation

How would evaluate the cause of this patient’s deterioration?


  • Thorough history: presenting complaint, fevers, sputum, calf pain, DVT prophylaxis, cancer history, previous TTE, recent medications, allergies
  • Examination: vital signs, localising signs of infection, rash
  • Bedside: ABG – gas exchange, lactate, ECG (ischaemia, s1q3t3, RBBB), CXR – consolidation, pneumothorax, heart failure, quick TTE, urine
  • Bloods: full-bloods – organ function, G+H in-case intervention required, septic screen, troponin
  • Imaging: CTPA, consider CT Abdo

What is a sub-massive PE?

Definition: PE with SBP > 90mmHg (without systemic hypotension) but evidence of right heart dysfunction or myocardial necrosis.

Evidence of RV dysfunction can be with:

  • ECG: new complete or incomplete RBBB, STE or depression and TWI in V1-4 +/- inferior leads
  • Echocardiography: features include RV dilatation and hypokinesis, interventricular septal flattening and paradoxical movement towards the LV, pulmonary hypertension, McConnell sign (regional RV dysfunction with free wall hypokinesis but apical sparing), tricuspid regurgitation
  • CTPA: RV dilatation
  • Biomarkers: elevated BNP or N-terminal pro-BNP

While evidence of myocardial necrosis is with an elevated troponin.

Patient’s with a sub-massive PE have a worse prognosis than those without RV dysfunction.

What is the role of systemic thrombolysis in patients presenting with sub-massive PE?

The use of thrombolysis in patients with sub-massive PE is controversial both in terms of patient selection and ideal dose. The rationale for its use is that it may:

  • Improve haemodynamics by increasing LV filling
  • Reduce the clot burden and thereby reduce pulmonary vascular resistance and the risk of chronic pulmonary hypertension
  • Prevent ongoing RV injury

The advantages of thrombolysis in sub-massive PE are:

  • It is readily available
  • Relatively cheap
  • Improves systemic haemodynamics
  • Quicker resolution of clot
  • Decreased recurrence of PE


  • Increased risk of haemorrhage
  • No proven mortality benefit
  • Evidence base not strong
  • Contra-indications include: prior ICH, active bleeding, ischaemic stroke within 3 months, intra-cranial malignancy or structural disease, recent neurosurgery or head trauma


  • PEITHO trial 2014
    • 1006 patients multi-centre RCT which compared full-dose thrombolysis + anticoagulation vs placebo + anticoagulation
    • No significant difference in mortality  or chronic pulmonary hypertension
    • Haemodynamic decompensation was significantly lower in the thrombolysis group but the risk of major bleeding was significantly higher
  • MAPPET-3 trial 2002
    • 256 patients with submassive PE compared full-dose thrombolysis + anticoagulation vs placebo + anticoagulation
      • Found that patients with thrombolysis had reduced in-hospital death or clinical deterioration requiring escalation of treatment
      • No difference in mortality or major bleeding
  • There are some trials that have examined the use of reduced-dose thrombolysis instead.
    • MOPETT trial in 2013 used half dose tpA in patients with sub-massive PE and found the patients with thrombolysis had a lower pulmonary artery systolic pressure at 28 months but no mortality difference or difference in risk of bleeding.

Alternatives to systemic thrombolysis include:

  • Catheter-directed thrombolysis
  • Anticoagulation alone
  • Surgical embolectomy.

The use of thrombolysis in sub-massive PE requires careful patient selection and consideration.

2. A 40-year-old previously well male is admitted to ICU for management of oliguric acute kidney injury accompanied by high fever with rigors, respiratory distress and headache. He has just returned from a brief tour of SE Asia. What are 5 likely differentials for this man’s presentation and what features on history would help you distinguish between them?

This patient likely has an infection which may be a specific overseas travel-related illness such as malaria, leptospirosis or dengue, or not specifically related to his travel such as influenza or bacterial meningitis.

Features on history that would help distinguish would be epidemiological information and information surrounding his presentation. 


  • Area of south-east Asia he travelled to
    • Travel to water areas (malaria),
  • Time of year
    • Rainy season – increased risk Dengue, winter (influenza)
  • Use of prophylaxis and protective measures
    • Mosquito repellants and nets: important for mosquito-borne illnesses such as malaria and dengue
    • Chemoprophylaxis for malaria such as doxycycline
    • Vaccination for influenza or meningitis
  • Activities
    • Freshwater swimming, exposure to livestock, water sports – leptospirosis
  • Unwell contacts
    • Influenza especially
  • Length of stay
    • Influenza 1 – 4 days
    • Meningitis 2 – 10 days
    • Dengue 3– 14 days
    • The incubation period for malaria is 7 – 30 days depending on the species
    • Leptospirosis 2 – 30 days


  • Mosquito bites: malaria, dengue
  • The pattern of illness:
    • Malaria: cyclical fever
    • Dengue: biphasic fever
    • Leptospirosis: biphasic illness – acute febrile phase with influenza-like illness for 2 – 9 days, a reprieve for 1-3 days followed by an immune phase
    • Meningitis: change in mental status, neck stiffness, nausea, rash
  • Other features
    • Dengue: headache, vomiting, myalgia, eye pain, rash, haemorrhagic manifestations, abdominal pain
    • Influenza: URTI symptoms, myalgia, malaise
    • Leptospirosis: conjunctival suffusion, rash

What are the clinical features of severe falciparum malaria and how would you diagnose it?

Clinical features:

  • On examination:
    • Fever that is cyclical
    • CNS: impaired consciousness, seizures, prostration, focal neurological deficits
    • Shock
    • Respiratory distress, pulmonary oedema
    • Jaundice
    • Recurrent or prolonged bleeding
    • Oligoanuria
  • On investigations
    • Blood tests:
      • LFTs: raised bilirubin
      • Coags: DIC, coagulopathy
      • FBC: severe anaemia, evidence of haemolysis (elevated LDH and reticulocytes, decreased haptoglobin), thrombocytopenia
      • Hypoglycaemia
      • ABG: metabolic acidosis, hyperlactatemia
      • UEC: acute kidney impairment
      • Haemoglobinuria
      • Hyperparasitemia  (> 2% of red blood cells parasitised)
  • CXR: pulmonary oedema


Suspected if there is fever and relevant epidemiologic exposure. Confirmed by:

  • Thick and thin films
    • Thick films: estimates the parasite load, more sensitive for detecting low-density parasitemia
    • Thin films: helps to identify the species
  • Rapid diagnostic tests are increasingly important in resource-limited settings as they give results within 15 – 20 minutes, are cheap, less intensive and require less training. They detect malaria parasite antigens so can confirm infection but give no information about the parasite load or whether this is a new or persistent infection. They are not useful for monitoring treatment.
    • An example for p. falciparum is histidine-rich protein 2

Briefly outline the treatment of severe falciparum malaria.


  • Resuscitation
    • May require intubation depending on the level of consciousness and respiratory function
    • Respiratory support with supplemental oxygen, NIV or invasive ventilation depending on the status
    • Full monitoring and haemodynamic support with adequate IV access, fluids and vasopressors
    • Treat seizures with benzos, evaluate for cerebral malaria or co-existing meningitis if the decreased level of consciousness or focal deficits – fundoscopy showing malarial retinopathy is pathognomic for cerebral malaria 
    • Admission to ICU
  • Specific
    • Artesunate or quinine (2nd line)
    • Adjunctive therapy with ceftriaxone (bacteremia is common) and paracetamol 1g QID for 24 hours (reduces risk of haemolytic AKI)
    • Exchange transfusion has been used but there are no clear consensus guidelines f on when it is suitable or the practicalities involved. Previous indications have been:
      • Parasitemia > 30%
      • Parasitemia > 10% with severe disease or failure to respond to treatment after 12 – 24 hours
  • Supportive
    • Monitor BSL regularly  especially if quinine given as it stimulates insulin secretion and can cause hypoglycaemia
    • Nutrition: ideally enterally
    • PPI
    • DVT prophylaxis: mechanical if severe coagulopathic
    • IDC – monitor fluid balance, routine indications for dialysis
    • Monitor parasite density initially every 12 hours then daily to confirm adequate response to treatment
    • Monitor and treat complications such as concomitant infections
    • Core temperature monitoring and treat fevers

3. 24 hours after a TOE to facilitate the treatment of chronic AF, a 60F presented to the ED with acute, severe chest pain. Obs are HR 120 SR, SBP 80mmHg improving to 110mmHg after 1L bolus of crystalloid, RR 32/min, sats 92% on 6L o2 via HM. What is your differential diagnosis and how would you evaluate her?

I am concerned that this patient has an oesophageal perforation secondary to the TOE although there are numerous other possible differentials unrelated to the procedure including:

  • Cardiovascular: acute myocardial infarction, aortic dissection, pericarditis, mural thrombus, myocardial stunning
  • Gastrointestinal: perforated peptic ulcer, severe pancreatitis, mesenteric ischaemia, cholecystitis/cholangitis
  • Respiratory: pneumonia with sepsis, pulmonary infarct, PE, pneumothorax

In order to evaluate her, I would simultaneously resuscitate this patient and perform a targeted assessment and investigations.


A – hypoxic on moderate fio2 and tachypnoea, evaluate airway, supplemental o2, may need intubation if unable to lie flat for CT no positive pressure ventilation without intubation, RSI induction

B – continuous sats monitoring, ECG/BP, IDC, auscultate chest, CXR ?effusion ?consolidation ?pneumothorax/pneumomediastinum

C – 2 x large-bore IV access, arterial line if time allows, judicious fluid resuscitation, vasopressor support initially peripherally if needed, ECG, surgical emphysema

D – analgesia, small boluses opiates, paracetamol, keep NBM, check BSL

E-check the temperature, insert IDC


Hx + exam: presenting complaint, co-morbidities, allergies, fasting status, neuro changes, radial-radial delay, abdomen ? benign


  • Bedside: ECG for signs of ischaemia, ABG/VBG to assess metabolic parameters and gas exchange, BSL, UA,
  • Bloods: full-bloods, G+H, troponin, septic screen, lipase
  • Imaging: CXR to assess for pneumomediastinum, pneumothorax, consolidation, likely CT chest/abdomen with contrast depending on findings
  • If pleural effusion may send of pleural fluid – the presence of food particles, pH < 6 and high amylase concentration, the culture of fluid

A CT scan confirms an oesophageal perforation. Outline your management of this situation.

This is an emergency situation.


  • Resuscitation and monitoring as outlined earlier
  • Specific: Surg review and source control
    • Surgical: primary repair, oesophageal diversion, resection and reconstruction (generally delayed until sepsis resolved), drainage and decortication of pleural effusion and mediastinal collections
    • Endoscopic: Covered oesophageal stenting if contained perforation, limited extra-luminal soiling, small perforation
    • Conservative: abx, jejunostomy for feeding and drains for collections
    • Follow up imaging to assess treatment result: CT gastrograffin swallow
  • Supportive care
    • Nutrition: NBM, PPI, TPN
    • Analgesia: opiates, regular paracetamol
    • Broad-spectrum antibiotics which cover anaerobic, gram-positive and gram-negative organisms (Tazocin)
      • Consider antifungals if an immunosuppressed or recent long hospital stay
    • Disposition: ICU or OT depending on the treatment plan
    • Update family and open disclosure about complication

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