The Deteriorating Ward Patient — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Margaret O'Sullivan is a 78-year-old retired teacher, admitted four days ago with community-acquired pneumonia, who has acutely deteriorated overnight with a rising NEWS2 from 3 to 9 over six hours. She has a background of ischaemic heart disease (a prior NSTEMI three years ago), chronic kidney disease stage 3 with a baseline creatinine of 140, type 2 diabetes on metformin and empagliflozin, hypertension, and moderate aortic stenosis. She lives independently with her husband. [1]

Her main problems are:

1. Septic shock from progressive pneumonia — refractory hypotension at 84 over 52, lactate 4.6, mottled peripheries, oliguric at 15 mL per hour.
2. New atrial fibrillation with rapid ventricular response at 128 — likely a complication of the sepsis, the fever, and the electrolyte disturbance.
3. Acute kidney injury with hyperkalaemia — creatinine risen from 140 to 210, potassium 5.8, oliguric.
4. Respiratory failure — type 1, SpO2 88 per cent on room air.
5. New delirium — a marker of severity and a management priority.
6. Significant comorbidity and the ceiling-of-care question — aortic stenosis, CKD, ischaemic heart disease, and diabetes. [1]

My immediate priorities are the ABCDE assessment with high-flow oxygen, cautious intravenous fluid resuscitation in smaller aliquots given her aortic stenosis, the Sepsis Six bundle with broad-spectrum antibiotics, treatment of the hyperkalaemia with calcium gluconate and insulin-dextrose, withholding the nephrotoxic and harmful drugs, and an urgent MET call for ICU outreach review given her refractory hypotension and the likely need for vasopressor support and possibly renal replacement therapy. I will also, in parallel, ask the family about an advance care directive and have an early, honest conversation about the ceiling of care." [1]

Examiner probing questions and model answers

Q1: "Walk me through your fluid strategy in a patient with septic shock and aortic stenosis." [1]

"The standard Surviving Sepsis Campaign 2021 recommendation is 30 mL per kilogram of crystalloid in the first three hours for sepsis with hypoperfusion [4]. But this patient has moderate aortic stenosis and ischaemic heart disease, which makes her vulnerable to fluid overload and acute pulmonary oedema from an uncritical large-volume bolus. My approach is to give smaller aliquots — 250 mL of balanced crystalloid over 15 minutes — and to reassess between each bolus for evidence of fluid responsiveness (a rise in blood pressure, a fall in heart rate, an improvement in capillary refill or mottling) and for signs of overload (a rise in JVP, new basal crackles, a fall in SpO2, increasing work of breathing). If she is not fluid-responsive or if she develops signs of overload, I have a low threshold to start an early vasopressor — noradrenaline via a central line — to restore the mean arterial pressure to above 65 mmHg. If I have access to dynamic assessment — a passive leg raise, a focused bedside echocardiogram, or stroke volume variation — I use it to guide the fluid. The principle: the guideline gives the total amount; the comorbidity dictates the rate and the aliquot size, and the reassessment between each bolus is what keeps the patient safe."

Q2: "Her potassium is 5.8. Walk me through your management of the hyperkalaemia." [1]

"The first step is to assess the ECG — at a potassium of 5.8 I would expect peaking of the T waves, and at higher levels I look for loss of P waves, widening of the QRS, and ultimately a sine-wave pattern that prefigures cardiac arrest. The management is in three tiers. First, myocardial membrane stabilisation — calcium gluconate 10 mL of 10 per cent intravenously over 5 to 10 minutes; this does not lower the potassium but it stabilises the myocardium within minutes and reduces the risk of dysrhythmia. Second, shift potassium into cells — insulin-dextrose (10 units of Actrapid in 50 mL of 50 per cent dextrose over 15 minutes) and a salbutamol nebuliser (5 to 10 mg); both take 15 to 30 minutes to work and lower the potassium by 0.5 to 1.0 mmol per litre. I monitor the blood glucose during and after the insulin-dextrose because of the risk of hypoglycaemia at 1 to 2 hours. Third, remove potassium from the body — this patient has acute kidney injury with a rising creatinine and is oliguric, so she is unlikely to excrete the potassium spontaneously; if the hyperkalaemia is refractory or recurs after the shifting therapy, she will need renal replacement therapy, which is itself an indication for ICU admission. I recheck the potassium and the ECG within 30 minutes of the initial therapy. The trap to avoid is treating the number without the patient — if the ECG shows widening of the QRS or a sine-wave pattern, the calcium gluconate is given first and urgently, before anything else." [1]

Q3: "She has new atrial fibrillation. Do you cardiovert, rate-control, or do nothing specific?" [1]

"My priority is to treat the cause of the AF, not the AF itself. In a patient with acute sepsis, fever, hyperkalaemia, and underlying ischaemic heart disease and aortic stenosis, the AF is almost certainly secondary to the acute illness and the sympathetic surge, and it will usually revert as the sepsis is treated and the electrolytes are corrected. I would NOT give a beta-blocker or a calcium-channel blocker in her hypotensive state — they will worsen the blood pressure and may precipitate cardiovascular collapse. If the AF is itself causing haemodynamic compromise that does not respond to the resuscitation — that is, if the blood pressure remains inadequate and the perfusion is worsening despite the fluid and the vasopressor — then my options are amiodarone 300 mg intravenously over one hour (a negative inotrope but less hypotension than a calcium-channel blocker, and appropriate for AF in the setting of structural heart disease) or, if she is peri-arrest, synchronised DC cardioversion. The teaching point is the order: treat the sepsis and the hyperkalaemia first, and the AF usually settles; specific antiarrhythmic therapy is reserved for the AF that is itself the haemodynamic problem. I would also anticoagulate her once the acute phase is resolving, because new AF carries a stroke risk and she will likely be in AF for more than 48 hours." [1]

Q4: "How would you decide whether she is for ICU?" [1]

"The decision is made by a senior clinician — ideally the treating consultant — in discussion with the patient (if she has capacity, which she may not, given her delirium) or her family, and with the ICU team. I weigh three things. First, the reversibility of the acute problem: the pneumonia is potentially reversible with antibiotics and organ support, which favours escalation. Second, her baseline function and quality of life: she is described as independent, living with her husband, which favours escalation; the picture would be different if she were bedbound in residential care with advanced dementia. Third, her expressed wishes: I ask the family, gently and early, whether she has an advance care directive, whether she has ever spoken about what she would want in this situation, and what she would consider an acceptable outcome. On the balance, a previously independent 78-year-old with reversible sepsis is, in most institutions and in my judgement, a candidate for a time-limited trial of ICU care — a defined period, perhaps 48 to 72 hours, of maximal support after which we reassess, and if the treatment is working we continue, and if it is not we refocus on comfort. I do not frame this as all-or-nothing; the trial of ICU is a defined, time-limited commitment with a clear review point. And I keep the family informed at every step — the honest, hopeful conversation that the sepsis is treatable, that the next two to three days will tell us whether the treatment is working, and that we will revisit the plan together." [1]

Q5: "What is the evidence that the rapid response system you are invoking actually works?" [1]

"The evidence is nuanced, and I carry it honestly. The MERIT study, the only cluster-randomised controlled trial, found that introducing the MET system increased emergency team calls from 3.1 to 8.7 per 1000 admissions but did not significantly reduce the composite primary outcome of cardiac arrest, unexpected death, or unplanned ICU admission [3]. The trial was underpowered, there was contamination, and the implementation period was short. The meta-analytic evidence is more favourable: Chan's 2010 systematic review of 18 studies found that rapid response teams were associated with a 33.8 per cent reduction in non-ICU cardiopulmonary arrests, though no significant reduction in overall hospital mortality [5]. My reading of the synthesis is that rapid response systems work — they reduce cardiac arrests, they change the safety culture of the hospital, they surface deterioration earlier, and they facilitate appropriate escalation — but the mortality signal is diluted by the patients for whom escalation is appropriately withheld, and by the before-and-after design of most of the studies. For this patient, the principle is not whether the system works in aggregate but whether calling the team now is the right thing for her — and it is."

Q6: "Give me the SBAR handover you would deliver to the ICU outreach team." [1]

"Situation: 'This is Dr Smith, the ward registrar. I am calling about Mrs O'Sullivan in bed 14, a 78-year-old woman admitted four days ago with community-acquired pneumonia, who has acutely deteriorated over the last six hours with a NEWS2 that has risen from 3 to 9.' Background: 'She has ischaemic heart disease with a prior NSTEMI, chronic kidney disease stage 3 with a baseline creatinine of 140, type 2 diabetes on metformin and empagliflozin, hypertension, and moderate aortic stenosis. She has been on IV benzylpenicillin and clarithromycin since admission.' Assessment: 'Her current observations are: respiratory rate 30, SpO2 88 per cent on room air and 92 per cent on 15 litres via a reservoir mask, heart rate 128 in new atrial fibrillation, blood pressure 84 over 52, GCS 14 with new mild confusion, temperature 38.7. Her lactate is 4.6, her creatinine has risen from 140 to 210, and her potassium is 5.8 with peaking of the T waves on the ECG. She is oliguric at 15 mL per hour. I have given high-flow oxygen, started the Sepsis Six with piperacillin-tazobactam, given 250 mL of crystalloid cautiously given her aortic stenosis, and treated the hyperkalaemia with calcium gluconate and insulin-dextrose.' Recommendation: 'I would like you to come and review her on the ward now. My concern is refractory septic shock with multi-organ failure — she is likely to need vasopressor support for the blood pressure, treatment of the hyperkalaemia that may include renal replacement therapy, and possibly non-invasive ventilation for the respiratory failure. I think she needs ICU admission, and I would like your assessment and the discussion about the ceiling of care given her comorbidities.'" [1]

Short Case Discussion

Bedside ABCDE assessment of the acutely unwell patient

Examiner instruction: "You are called to the ward to review a patient the nursing staff are concerned about. The only information you have is that he 'looks unwell.' Describe your systematic approach to the assessment, the first interventions you would make, and the key questions you would ask." [1]

Candidate's model answer: [1]

*"My approach follows the ABCDE structure, treating life-threats in the order they are found. Before I touch the patient, I take five seconds at the end of the bed: is he in distress, is he breathing comfortably, is the colour normal, is the conscious level appropriate? The experienced clinician's gestalt of 'sick or not sick' in the first five seconds is rarely wrong, and it sets the urgency for everything that follows. [1]

I then review the observation chart — the full vital sign set and the NEWS2 trajectory over the last 12 to 24 hours. The chart tells the story; the parameter that is driving the score and the rate of change are the two pieces of information I weight most heavily. A rising trend is deterioration regardless of where the absolute value sits. [1]

Airway. Is the airway patent? I look, listen, and feel — chest movement, breath sounds at the mouth, expired air. If there is obstruction — snoring, gurgling, stridor, see-saw breathing — I do basic manoeuvres (head tilt, chin lift, or jaw thrust if cervical spine is a concern), insert an airway adjunct (oropharyngeal if unconscious with no gag, nasopharyngeal if the gag is intact), and suction. If the airway cannot be secured, I call for senior airway help immediately. [1]

Breathing. Respiratory rate, SpO2, chest expansion, use of accessory muscles, percussion note, auscultation. I give oxygen to any acutely hypoxaemic patient — high-flow via a reservoir mask for the critically ill, titrated to a target of 92 to 96 per cent (88 to 92 per cent for the chronic CO2 retainer). I send an arterial blood gas if there is any concern about ventilation or acid-base. The respiratory rate is the leading indicator; a high rate is the earliest sign of deterioration and the SpO2 is a lagging marker. [1]

Circulation. Heart rate and rhythm (12-lead ECG and continuous monitoring), blood pressure, capillary refill, peripheral and central pulses, JVP, skin temperature and mottling, urine output. Two large-bore cannulae, a fluid challenge of balanced crystalloid, and the cause-specific therapy. I always interpret the blood pressure against the patient's baseline — a systolic of 110 in a chronic hypertensive is a significant drop. [1]

Disability. GCS or AVPU, pupils, and — critically — a bedside blood glucose in every patient with an altered conscious level. Hypoglycaemia is rapidly reversible and is missed catastrophically if not measured. [1]

Exposure. Temperature and a full examination — the abdomen, the skin, the lines, the wound, the peripheries. I review the drug chart — every drug, every dose, every recent change. [1]

In parallel with the ABCDE, I take a focused history from the patient, the nursing staff, and the chart: the admission diagnosis, the comorbidities, the recent course, the events leading to the deterioration. And I make the decision early: is this a patient I can manage on the ward, or do I need to call for help? The threshold for calling is set lower than the threshold for arrest — if I am worried, I call, and the worried criterion is built into every MET system for exactly this reason."* [1]

Examiner: "What is the single most important piece of advice you would give a junior doctor about recognising the deteriorating patient?" [1]

"Measure the respiratory rate, document it, and act on the trend. The respiratory rate is the earliest, the most reliable, and the most frequently omitted vital sign. A rising respiratory rate is the body's first measurable response to hypoxia, acidaemia, pain, sepsis, and metabolic upset. Schein's 1990 study showed that 84 per cent of in-hospital arrest patients had documented deterioration in the eight hours before arrest, and the dominant antecedents were respiratory [1]. The junior doctor who measures the respiratory rate at every observation, who watches the trend, and who escalates when the trend is rising — even if the absolute value is not yet catastrophic — has intercepted most preventable ward arrests at their origin. The second piece of advice: never let a normal blood pressure reassure you into inaction. Blood pressure is a late marker; by the time it falls, the patient has exhausted compensation. The third: call for help early. It is always acceptable to call, and the call that turns out to be unnecessary costs minutes; the call that should have been made and was not costs a life."