ED - Short Cases Flashcards
- Where should Barry be assessed in the Emergency Department?
- What bedside investigation should be undertaken as an emergency ?
- Barry presents with chest pain to an Emergency Department. He should be triaged as an NTS 2 and placed in a monitored environment while he is being assessed for life threats. [His vital signs are stable]. An intravenous line should be placed.
- An ECG should be performed within 10 minutes of arrival.
Interpret Barry’s ECG.
What needs to be done?
- The ECG demonstrates an inferior STEMI (note the St segment elevation in leads II, III and aVF with reciprocal T wave inversion in lead V2, V3.
- This is a life threatening condition. While he appears to be currently stable , time critical intervention can influence the outcome. A team based approach with simultaneous history and examination is required as well as organising the next urgent phase- acute revascularistaion – in this case via PTCA as a cardiac catheter lab is imminently accessible. He should be placed on oxygen, given aspirin 300mg PO and a decision made urgently regarding thrombolysis or PTCA.
What is a V4r in the context of ECGs?
- What is the significance of cardiovascular disease in Aboriginal Australians?
- List 4 risk factors for ischemic heart disease
- Cardiovascular disease is the major cause of premature death among adult Aboriginal Australians..”
- Age specific death rates from Cardiovascular disease in Aboriginal people is estimated to be 4-7 times the rates in the general populations.
- In the study [1] the risk factors for ischaemic heart disease were identified:
1. Diabetes mellitus
2. Overweight or obesity
3. Smoking
4. Hypertension
What do you consider is the most likely diagnosis?
= Pulmonary embolism
This is the stand out concern based on the pre-existing history of a below knee DVT More than 70% of all PE originate in the pelvis and deep veins of the lower extremities.
- What are 5 risks for a VTE?
- When is a D-dimer useful?
- What is the estimated mortality from an untreated PE?
Risks for VTE - Major risk factors for carrying a relative risk of 5-20 for VTE:
1. Recent surgery < 4 weeks
2. Immobilisation (or bed rest > 3 days)
3. Post partum ( for up to 6 weeks)
4. Malignancy
5. History of VTE
- Authors comment : note morbid obesity does not make the list in most textbooks but I think it will do one day!
- Here’s the problem for clinicians – this case is pretty straightforward – it’s the ones who have non specific symptoms that make the diagnosis elusive.
- Note the D –dimer in combination with Wells criteria scoring systems can only be used safely in patients who have a LOW pre-test probability.
- The mortality from untreated PE is estimated to be approximately 30%
What is the role of the following investigations in the diagnosis of PE:
- ABG?
- Troponin?
- ECG?
- D-Dimer?
- CXR? 3 Classical Signs?
- ABG in PE - PIOPED study in 1990 – demonstrated that ABG is a poor diagnostic test to rule out PE- remember this next year when the imaging dept ask you for ABG on a patient with Sats of 97% on room air. A normal arterial blood gas does not rule out PE.
- Troponin - Troponin can be raised in PE. So it is important to think about – thus an elevated troponin in this setting does not indicate an acute coronary syndrome- those patients who have a troponin rise with their PE have a worse outcome overall.
- ECG changes – non specific- S1Q3T3 represents acute core pulmonale and is not pathognomonic of PE – although its presence should make you think “ why is it so”.
- D-dimer - A raised D dimer has a poor positive predictive value but a strong negative predictive value in the diagnosis of PE- this means in a low risk patient with a negative D dimer – PE is unlikely ( or about 98% chance!)
What 11 symptoms and signs are associated with pulmonary embolism?
Would a fever of 38.2 C make PE less likely?
Note a fever above 39.5C is not associated with PE
Explain the principles of the Wells classification.
What imaging studies could you order in suspected PE?
1) CTPA – involves more radiation than V/Q but has the advantage of diagnosis of alternative causes in some instances.
2) V/Q scan – increasingly more sensitive in recent years- especially useful when CTPA may be risky or contraindicated eg renal failure or allergy to contrast
- What is the most likely diagnosis ? What are your differential diagnoses? (5 minimum)
- What is your management for this patient -Examination?
Acute pyelonephritis is the most likely diagnosis.
Other differential diagnoses include:
1. UTI
2. Ectopic pregnancy
3. Pregnancy
4. Ruptured ovarian cyst
5. Appendicitis etc
- Which investigations would you order for this patient with a suspected Acute pyelonephritis?
- What is your treatment? (3)
Treatment (TG: Antibiotic guidelines)
1. Analgesia- panadeine forte
2. Nausea/vomiting- ondansetron
3. Antibiotics- Mild cases- Trimethoprim 300mg PO once daily for 10days or Augmentin duo forte 875mg +125mg PO BD 10days, or Cephalexin 500mg PO QID 10days. Severe cases- Gentamicin 4-6mg/kg IV 1 dose. + amoxicillin/ampicillin 2g IV 6hrly.
- What is the most likely cause of this condition (acute pyelonephritis)?
- What are the potential consequences if this condition is not treated? (3)
- 3 Risk factors for UTI/Acute Pyelo in females?
= E. Coli. Other likely organisms include Gram –ve (P. mirabalis, Klebsiella spp., P. aeruginosa) and Gram +ve (Coagulase negative staphylococci, Enterococci spp, Group B strep, S. Aureus)
- Imaging protocol for suspected Acute Pyelonephritis?
- What are the 6 diagnostic imaging indications?
Diagnostic Imaging Indications in Acute Pyelonephritis
1. When the diagnosis is uncertain/equivocal
2. If obstruction of the collecting system is suspected, investigation is required to prevent destruction of the renal parenchyma and irreversible loss of renal function.
3. Patients who have an underlying anatomical predisposition that may predispose to complications of acute pyelonephritis (eg known congenital abnormalities).
4. Patients with recurrent acute pyelonephritis
5. ‘High Risk’ patients who are more susceptible to occult infection or complications of acute pyelonephritis. This includes individuals with diabetes mellitus, elderly patients, patients who are immunosuppressed or on immunosuppressant therapy and renal transplant patients
6. Patients who fail to respond to culture sensitive intravenous antibiotics after 72hrs of therapy.
- What is the role of Ultrasound in suspected Hydronephrosis/Pyonephrosis?
- What is the role of CT?
Role of U/S
- In the adult, hydronephrosis/pyonephrosis is usually due to acute or chronic obstruction secondary to calculus, tumour, stricture or congenital anomaly with super-imposed infection.
- Ultrasound is sensitive in the detection of pelvi-calyceal dilation. When pyonephrosis is present, echos and septations secondary to gas forming bacteria or debris may be seen 3-4.
- Further imaging may be required prior to/or following decompression via a percutanoeus nephrostomy or retrograde ureteric stent placement, in order to establish the cause of obstruction. In this case a CT may be warranted.
Acute Pyelonephritis
- What is it?
- S&Ss?
- Cause?
- Diagnosis?
What is Wellens syndrome?
- Wellens syndrome is a pattern of ECG T wave changes associated with a proximal LAD lesion.
- These patients are very high risk for developing acute myocardial infarction.
- Investigating with an exercise stress test is dangerous as the precipitant increase in myocardial demand can precipitate a fatal AMI.
- The syndrome was first described in 1982 following the observation that inverted T wave changes in the precordial leads was strongly associated with a early large anterior myocardial infarction. This identified group of patients have a better outcome with early angiography and selective angioplasty or surgical treatment.
- About 3⁄4 of these patients will develop an anterior myocardial infarction – even with medical management.
- What would be a differential diagnosis for complaint in a 67 year old? (6)
- What 2 life threatening conditions must you consider?
An elderly man who presents with an acute onset of back pain should prompt a search for a life threatening cause. Always make sure your examination is thorough and complete- don’t accept attempting to short cut your examination- examine on a trolley.
The potentially acute life threatening causes include:
1. Abdominal aortic aneurysm
2. Aortic dissection
Other causes for pain would include:
1. Lumbosacral disease
2. Mechanical back pain
3. Malignancy
4. Spinal stenosis
5. Intervertebral disc herniatio
6. Cauda equina syndrome
- When is resection or endovascular stenting recommended for abdominal aortic aneurysms?
- What are 3 ways an AAA may present?
- What are the typical sites of presentation of AAA?
- Classic triad of findings?
- Differentials?
- Abdominal aortic aneurysms can be difficult to diagnose if not considered. Most abdominal aortic aneursyms are without symptoms until complication. The risk of rupture depends on size of the aneurysm.
- Resection or endovascular stenting is recommended for aneurysms of 5cm or more in size.
3 ways AAAs present:
1. Asymptomatic - incidental finding during examination.
2. Symptomatic – acute back pain /episode of syncope
3. Ruptured- collapse with hypotension
- What percentage of AAAs are infrarenal?
- 90% of AAA are infrarenal.
Outline the immediate management of Gary upon arrival in the ED.
- List 5 Major causes of upper GIT bleeding?
- List the signs of chronic liver disease/acute failure?
List Major causes of upper GIT bleeding
1. DU-25%
2. Gastric ulcer 20%
3. Mallory Weiss tear
4. Varices
5. Erosive gastritis/oesophagitis
Clinical signs of chronic liver disease
1. Spider naevi
2. Ascites
3. Gynaecomastia
4. Hepatosplenomegaly
5. Palmar erythema
6. Testicluar atrophy
7. Dilated abdominal veins = caput medusa
8. Hepatic flap (acute)
- What is the most likely cause for his presentation?
- How would you manage this life threatening illness?
- What is a minimum period of observation after treatment and why?
In which patients in ED would we look for hypoglycaemia?
= in all patients with altered mental status, focal neurological signs or seizures, diabetic patients.
What are the clinical features of hypoglycaemia?
What causes hypoglycaemia?
- In the diabetic patient? (2)
- In the non-diabetic patient? (7)
What are the treatment options?
- What would be the differential diagnosis you would consider?
- Which of these would be the most concerning?
Which of these would be the most concerning?
The infective complications would be the most important to consider.
What investigations would help in your initial management?
As always there is no substitute for a careful history and detailed examination but useful investigations would include:
1. FBP- looking for raised WCC suggestive on infection
2. CRP- useful to suggest an infective cause
3. Lumbar spine Xrays ? – note the history of trauma but the yield from these will usually be low
Changes due to infective causes will usually not be evident from plain xray - Need MRI.
Take home message: Second presentations to ED warrant a careful ‘ start from the beginning again approach. Be cautious in the label given to a patient. While back pain is a common cause of presentation – care is required to avoid missing serious treatable causes.
- What are 12 clinical features that would suggest chronic alcohol abuse?
- What are the clinical features of alcohol withdrawal? (4)
Clinical features of chronic alcohol use:
1. Tremor
2. Jaundice
3. Rosacea
4. Parotid swelling
5. Rhinophyma
6. Hepatomegaly
7. Spider naevi
8. Ascites
9. Muscle atrophy
10. Peripheral neuropathy
11. Ataxia
12. Cerebellar dysfunction
What are the life threatening complications of alcohol withdrawal?
How is alcohol withdrawal managed?
- Controlling symptoms? (5)
Control of symptoms
1. Clinical diagnosis but need to exclude other significant co-morbid illness.
2. Benzodiazepines (diazepam) is the agent used to control psychomotor agitation and prevent the progression more severe withdrawal. Note – the doses of diazepam that may be required in some patients will be high.
3. Occasionally mechanical restraint may be need for brief periods [employing clear guidelines]
4. Correct volume deficits- normal saline is the most useful in this regard.
5. Thiamine and glucose should be given to prevent Wernicke’s encephalopathy.
How do alcohol dependent patients end up in ED?
- What is the most likely diagnosis?
- What is the first thing you need to establish?
- Should you admit her?
- Interpret her VBG?
- What is MUDPILES?
This is a pretty typical presentation of diabetic keto acidosis. DKA is characterised by elevated BSL and ketonaemia. Your initial task is to resuscitate the patient and determine the most likely cause of the diabetic ketoacidosis (DKA) and to provide specific therapy if required. In this case the inability of the patient to recall their recent BSL results suggests perhaps poor awareness of control and the inability to tolerate diet has been the precipitant. The presence of an intercurrent upper respiratory infection may have been a precipitant. In view of the risk of a lower respiratory infection a CXR would be a useful investigation. All patients with established DKA will require admission. Careful monitoring of vital signs is required, ECG (high incidence of occult myocardial ischaemia and may be the precipitant.) Regular clinical and biochemical assessment. Remember this condition has a mortality in some series of 8% , so ask for help early.
What are the general principles of DKA management? (5)
Outline a classification of severity of DKA?
Outline the initial management of a patient with DKA?
Once a DKA has been corrected, how should this patient be monitored?
What is the definition of febrile neutropaenia?
- List 4 risk factors for febrile neutropaenia?
Risk factors for febrile neutropaenia include:
1. Post-chemotherapy - high risk if haematological malignancy, age> 60 years, incomplete cancer remission, significant comorbidities, significant mucositis, high dose of steroids
2. Post-transplantation
3. Chronic granulomatous disease
4. Clozapine-induced agranulocytosis
When should you suspect febrile neutropaenia?
What is the assessment to evaluate a patient with suspected neutropaenia?
- Clinical examination? (9)
- Investigations? (11)
Suspect neutropaenia in any haematology/ oncology patient that has received chemotherapy (oral or intravenous) within the last 14 days or has a history of recurrent neutropenia or has any of the above listed risk factors.
Outline the management steps for a patient with Febrile Neutropaenia?
Key Points
- Early identification of at risk patients
- Rapid empirical initiation of broad-spectrum IV antibiotics and source control is essential.
- The optimal antibiotic regime remains controversial.
- Non-infectious causes of fever are common in patients with haematological malignancy but often difficult to distinguish from infective causes acutely, therefore, treat all patients empirically.
- What do the physical signs on examination suggest as the likely cause? (6)
- What does the CXR show?
- What diagnostic and therapeutic procedure is required? 2 types?
- What specific investigations would you order? (6)
= Pleural effusion right side
Examination Findings may include:
1. Dullness to percussion
2. Decreased tactile fremitus
3. Reduced chest expansion or side of effusion
4. Diminished or inaudible breath sounds
5. Focal bronchial breathing at the superior aspect of the effusion
6. Pleural friction rub
- CXR demonstrates a large right sided pleural effusion. No lung lesion is identified.
- Definition of Pleural effusion?
- What are the common causes for pleural effusion and a classification system?
Definition of Pleural effusion: an abnormal collection of fluid in the pleural space resulting form excess fluid production or decreased absorption.
- What would you consider as possible causes for Mary’s pain? (9)
- What investigations would you order?
Abdominal pain in the elderly is often the symptom of a serious disorder. In contrast to younger patients elderly patients who present to the emergency department are more likely to have a surgical disease. A diagnosis that requires surgery is about 2 fold more prevalent but mortality is increased 10 fold over a younger cohort.
What do you think is the likely cause?
- What investigations might be of assistance and why?
- What further management would you arrange?
- What advice would you give to the patient?
- What is the likely cause of Pauline’s hyperkalaemia?
- In which groups of patients is this medication more likely to have this effect?
- How would you manage this lady considering there are no ECG changes?
- Pauline’s hyperkalaemia is likely caused by the spironolactone due to it being a potassium sparing diuretic. Renal function should also be assessed due to her hypertension.
- The elderly, diabetics, those with renal disease, severely ill patients and those with inadequate fluid intake
- The most important action is to cease the spironolactone. Consider a resin to bind K+ in the gut e.g. Calcium Resonium. Rehydrate her with IV normal saline and consider other measures if she is symptomatic or there are ECG changes. Monitor her for ECG changes.
- Which of her medications are for hypertension and how do they act?
- List 9 Causes of Hyperkalaemia?
Pauline is on 4 medications for hypertension;
1. Amlodipine – calcium channel blocker
2. Almesartan – angiotensin II antagonist
3. Spironolactone – aldosterone antagonist
4. Moxonidine – centrally acting alpha2 adrenoceptor agonists
- What signs and symptoms may hyperkalaemic patients present with?
- What 5 ECG changes are you looking for when hyperkalaemia is present?
- Hyperkalaemia can often be asymptomatic but cause anxiety, irritability, confusion, nausea, diarrhoea, abdominal distress, weakness, chest pain, palpitations and cardiac arrhythmias (sudden death).
- ECG changes to be looked for are:
1. Tall “tented” T waves (peaked)
2. Small or absent P waves
3. Increased PR interval
4. Widened QRS complex
5. “sine wave” pattern and then ventricular fibrillation
- What is the definition of severe hyperkalaemia?
- What is the management of severe hyperkalaemia? (7)
Severe hyperkalaemia is a serum potassium > 6.5 mmol/L or evidence of cardiac hyper excitability.
What exam findings are you looking for?
- What investigations would you order for this patient?
- Diagnosis?
Investigations:
1. Non-invasive monitoring (ECG and blood pressure monitor) attached.
2. Analgesia - He is given simple analgesia (ibuprofen and codeine) with good relief of his pain.
2. ECG: Sinus tachycardia, normal axis, normal intervals and segments.
3. Laboratory investigations: FBC, creatinine, electrolytes within normal limits, Trop T negative.
4. Chest X-ray
Diagnosis: (spontaneous) pneumomediastinum secondary to marijuana smoking.
What is the treatment for this patient? What advice should he be given?
Treatment
Damien was given high flow oxygen and was observed in ED for 4 hours until his pain had resolved and his vital signs had normalised. He was discharged home with a script for panadeine and ibuprofen. On discharge he was also advised:
1. Not to smoke marijuana again!!!
2. Avoid any Valsalva manoeuvres
3. To return to ED if any shortness or breath or fevers should occur.
4. Not to fly in an aeroplane for the 6 weeks pending review.
- How does a pneumomediastinum develop and what are the risk factors?
- What are the clinical features?
Symptoms of pneumomediastinum:
1. Retrosternal chest pain
2. Less frequently shortness of breath
or subcutaneous emphysema with tracking of air into the chest wall, neck, face, abdominal wall and scrotum.
On cardiac examination a “crunching” sound may be heared during systole, which is called Hamman sign.
- List 7 Differential diagnoses for retrosternal chest pain?
- List 3 possible complications?
- How is pneumomediastinum managed?
Differential diagnoses for retrosternal chest pain:
1. Myocardial infarction
2. Pericarditis
3. Gastroesophageal reflux
4. Pulmonary embolism
5. Pneumothorax
6. Pneumonia
7. Boerhave’s syndrome (oesophageal rupture)
What other questions would you like to ask ?
What do you look for on examination of this patient?
What is the most likely diagnosis? What are your differential diagnoses? (3)
The most likely diagnosis is Herpes Zoster Oticus (Ramsay Hunt Syndrome type 2) with trigeminal nerve distribution rash. In this case there is NO facial paralysis or weakness involved, only one- sided rash. It is a disorder caused by reactivation of herpes zoster virus in a nerve cell bundle called the geniculate ganglion. The symptoms and signs include acute facial nerve paralysis, otalgia, taste loss in the front two-thirds of the tongue, dry mouth and eyes, and eruption of a erythematous vesicular rash in the ear canal, the tongue, and/or hard palate.
Differentials - 1. Otitis externa, 2. Cellulitis, 3. Allergic reaction- insect bite/foreign agent/toxin.
What is the management of Herpes Zoster Oticus (Ramsay Hunt Syndrome type 2) with trigeminal nerve distribution rash?
- 3 investigations?
- Tx?
- Role of Steroids?
4 Possible complications?
In this case the diagnosis was made clinically. However consider:
1. Blood tests- FBC, UEC
2. Swab of a lesion- PCR or viral culture.
3. Serology for VZV IgM antibody.
Mx: Aciclovir, Valciclovir, Famciclovir analgesic- panadeine forte
Consider imaging- CT to find another cause of facial paralysis
Role of steroids? - A number of placebo-controlled trials evaluating acyclovir alone compared to antiviral therapy plus glucocorticoids did not demonstrate any benefit of combination therapy on quality of life or the incidence of Post herpetic neuralgia.
- What do you think is the diagnosis?
- What investigations would you order?
- What needs to happen for ongoing management?
- The history of cramping abdominal pain and absolute constipation suggests a bowel obstruction. Given the absence of abdominal distension it is likely to be a high abdominal obstruction. Your abdominal examination would include a careful scrutiny of hernial orifices.
- The AXR you order confirms what you suspected. The film shows multiple air-fluid levels in keeping with a mid small bowel obstruction.
- As part of your management you would insert an intravenous line for rehydration with normal saline initially and then with additional supplements as dictated by the serum electrolytes. A nasogastric tube will help to decompress the small bowel and alleviate further vomiting. Referral to a surgical unit and admission is required. His return flight scheduled for the next day should be cancelled.
- What would likely differential diagnosis in this patient? (5)
- What clinical features would help in arriving at a diagnosis?
The presence of gradual onset of shortness of breath would make the following possible inclusions:
1. Pulmonary embolus - particularly relevant given the history of carcinoma
2. Pericardial effusion
3. Large pleural effusion- would expect to detect on clinical examination
4. Pneumonia
5. Pneumothorax- somewhat atypical in the absence of signs and a normal CXR 2 days earlier
- What immediate investigations would you undertake and why? (3)
- What might you expect to see on these if she has a pericardial effusion?
- What is the investigation of choice to identify pericardial effusions?
- What is th enormal volume of fluid in the pericardial space?
- How are pericardial effusions treated?
- Symptoms?
After assessment for life threats to the airway, breathing and circulation the useful investigations would be:
1. ECG - This demonstrate electrical alternans- which is a rare manifestation of cardiac tamponade. The ECG characteristically shows decreased electrical voltage.
2. CXR - A chest x-ray in this case showed a widened cardiac silhouette.
3. Cardiac US - A bedside ultrasound in the ED demonstrated a significant pericardial effusion.
