33. A 59‐year‐old man who has end stage kidney disease due to diabetic nephropathy presents to haemodialysis centre for dialysis. He has missed his previous dialysis because he is worried about contracting COVID‐19 at the dialysis centre. He collapses just before commencing dialysis. CPR is started, ECG shows ventricular tachycardia, and VBG shows a potassium level of 7.9 mmol/L [3.5–5.2].
34. A 53‐year‐old man known to have cirrhosis due to alcoholic hepatitis is admitted to the Acute Medical Unit after binge drinking. He has been given intravenous thiamine and 5% dextrose infusion. He is found to have an irregular and difficult to palpate pulse with a BP of 110/70 mmHg. His cardiac monitor shows intermittent runs of the following rhythm.
35. An 85‐year‐old man is transferred from a peripheral hospital due to a fracture of neck of right femur. He has been given analgesia, settled in the ward and is fasting and waiting for surgery. He is a fit farmer apart from stage 3B CKD. However, the nurse finds him unconscious 4 hours later. He is afebrile, BP 120/80 mmHg, HR 76 bpm, respiratory rate 8/min, SaO2 90% on 6 L of oxygen. He has bilateral pin‐point pupils.
Answers
1. Answer: D
Acute Respiratory Distress Syndrome (ARDS) is a heterogenous syndrome with symptoms of tachypnea, refractory hypoxemia, and diffuse opacities on CXR or CT chest. More than 85% of patients with ARDS have risk factors such as pneumonia, aspiration of gastric contents, and sepsis. Other risk factors for ARDS include pulmonary contusion, inhalation injury, near drowning, non‐thoracic trauma, haemorrhagic shock, pancreatitis, major burns, drug overdose, transfusion of blood products, cardiopulmonary bypass, and reperfusion oedema after lung transplantation or embolectomy.
Direct or indirect insult to the alveolar structure causes alveolar macrophage activation. This leads to the release of pro‐inflammatory mediators and chemokines that attract neutrophils and monocytes. Toxic mediators are released by activated neutrophils causing alveolar injury, leading to loss of barrier function, interstitial, and intra‐alveolar flooding. Expression of tissue factor mediated by tumor necrosis factor then promotes platelet aggregation, intra‐alveolar coagulation, and hyaline‐membrane formation.
In patients with severe ARDS, mortality is up to 46%. Long‐term sequelae for the survivors of ARDS include depression, skeletal‐muscle weakness, post‐traumatic stress disorder, and cognitive decline. Identification and treatment of the underlying cause(s) of ARDS is the first priority in the care of the patients with this condition.
The volumes of the aerated lungs are reduced in patients with ARDS. Using lung‐protective invasive mechanical ventilation with lower tidal volumes and airway pressure has been reported to reduce ventilator‐associated lung injury and mortality. Avoidance of fluid administration following reversal of shock has been shown to reduce mortality in a large randomised trial. IV albumin administration was not associated with reduced mortality in a large randomised trial in patients with ARDS. Currently, no pharmacologic therapy has been shown to reduce short‐term or long‐term mortality in patients with ARDS. A recent trial shows that infusion of muscle relaxant for 48 hours may improve oxygenation but does not improve mortality. Placing the patient in the prone position for moderate to severe ARDS may reduce mortality. Introducing inhaled nitric oxide therapy improves oxygenation but does not improve mortality.
Distinguishing between initial fluid resuscitation for shock and maintenance fluid therapy is important. Early aggressive resuscitation for associated circulatory shock and its associated remote organ injury are essential. However, several small trials have demonstrated improved outcome for ARDS in patients treated with diuretics or dialysis to promote a negative fluid balance in the first few days. Primary ARDS due to aspiration, pneumonia, or inhalational injury can be treated with fluid restriction. Secondary ARDS due to sepsis or inflammation requires initial fluid and potential vasoactive drug therapy to stabilize the patient.
An ARDS Clinical Trials Network study of a fluid‐conservative strategy versus a fluid‐liberal strategy in the management of patients with ARDS found no statistically significant difference in 60‐day mortality between the two groups 72 hours after presentation with ARDS. However, patients treated with the fluid‐conservative strategy had an improved oxygenation index and lung injury score and an increase in ventilator‐free days, without an increase in non‐pulmonary organ failures.
Thompson B, Chambers R, Liu K. Acute Respiratory Distress Syndrome. New England Journal of Medicine. 2017;377(6):562–572.
https://www.ncbi.nlm.nih.gov/pubmed/28792873
2. Answer: C
This patient’s clinical presentation and signs are consistent with cardiac tamponade which is a rare complication after pacemaker insertion. The diagnosis of cardiac tamponade is clinical and requires prompt recognition. Echocardiogram is the best imaging modality to use at the bedside, as it can confirm the presence of a pericardial effusion, determine its size, and whether it is causing compromise of cardiac function such as right ventricular diastolic collapse, right atrial systolic collapse, plethoric inferior vena cava (IVC). The commonest ECG finding of cardiac tamponade is sinus tachycardia. ECG may show low voltages or electrical alternans, which is the classic ECG finding in cardiac tamponade. A CXR may show an enlarged heart and may strongly suggest pericardial effusion if a prior CXR is available for comparison. CT chest can also detect pericardial effusion.
Differential diagnosis includes large pleural effusion, pneumothorax, pulmonary embolism, constrictive pericarditis, CCF, and shock.
Cardiac tamponade is a medical emergency. The urgent treatment of cardiac tamponade is the removal of pericardial fluid/blood to relieve the pressure surrounding the heart. This can be done by performing a needle pericardiocentesis at the bedside, performed either using traditional landmark technique in a sub‐xiphoid window or using a point‐of‐care echocardiogram to guide needle placement in real‐time. Surgical options include creating a pericardial window or removing the pericardium.
Complications of pacemaker insertion may occur during the immediate or early post‐insertion period and can be related to (ii) venous access (pneumothorax, haemothorax, air embolism, haematoma, arterial puncture, wound healing problems, infection, pain), (ii) the pacemaker lead (cardiac perforation, tamponade, malposition or dislodgement of the lead), (iii) or the generator device. Late complications are related to infections, thrombosis, endocarditis, pulmonary embolism, superior vena cava (SVC) syndrome (due to thrombus formation and/or fibrosis of the pacing wires within the SVC), and pericarditis.
Mahadevan V, Agrawal H. Cardiac tamponade – Symptoms, diagnosis, and treatment | BMJ Best Practice [Internet]. Newbp.bmj.com. 2019 [cited 22 August 2019]. Available from: https://bestpractice.bmj.com/topics/en-gb/459
3. Answer: D
Carbon monoxide (CO) poisoning causes a large number of deaths due to intentional