WSPS is proud to introduce the Physicians Challenge!
Every month, we will post questions from a diverse range of specialties and perspectives. Give them a crack, and you may just win a prize in our monthly draw! We will post the answer and source of any materials used at the end of each challenge week.
Check our Facebook page for the latest Physicians Challenge.
Physicians Challenge 20: Spotty Child
You're the ED reg and you've just finished explaining to an intern why you don't order a D-dimer on every patient, "just in case they have a DVT." You're walking to the tearoom for a coffee and to your dismay, another intern stops you. He is worried about a child and you agree to take a look.
Alexis is a 15 year old boy who has had severe vomiting and diarrhoea for the past day. Today, he has been confused since he woke. He's complaining of fevers and a sore throat which he's had for the past 5 days. He's also had a poor appetite over the last few months and has lost some weight. His medical history is unremarkable.
You see a toxic looking child.
RR 48 BP 80/30 Temp 37.9
GCS 12 (M5 V4 E3)
Poor cap refill, cold and clammy peripheries
Skin appears mottled and pigmented
Heart, lung and abdo exam otherwise normal
The boy's face appears as below:
1. What would you like to do once you've completed the examination?
2. What investigations would you like? Justify your response.
3. What is your provisional diagnosis? Justify your response.
4. How are you going to manage this child?
Physicians Challenge 19: Big Belly
A 36 year old woman presents with weight gain of 14kg in the last 18 months. She has noticed that her menses have been irregular, and her mood has consistently been low. This has been accompanied by lack of motivation and anhedonia for the last few months. She has also noticed that she bruises easily and on examination, you see the following appearance of her abdomen. You also note predominantly central obesity.
1. What further questions are important to ask?
2. What is your provisional diagnosis?
3. What key investigations would you like to perform to aid diagnosis and management of this condition?
Physicians Challenge 18: Mrs Crab
Mrs Crab is a 66-year-old woman who presents to ED following fall on right arm after feeling light-headed. Her family report her having a 2-month history of fatigue, loss of appetite and weight, absent-mindedness, and nocturia. Her vital signs are normal, and she appears dehydrated. There are no other significant findings on examination apart from a deformity of the right mid-humerus with swelling.
FBC- Hb 92g/L
EUC- Creatinine 180mMol/l (normal 50 – 120 mMol/l)
CMP- corrected Calcium 3.25 mmol/L (normal 2.20-2.55)
X-ray of right humerus is shown.
1) What further investigations are required for hypercalcaemia?
2) What is the most likely diagnosis?
3) What is the immediate management?
Physicians Challenge 17: Impressing the Consultant
You are at the hospital on your ICM day and are keen to show Dr Keat how well you have learned your physical examinations by memorising Talley & O'Connor. A 65 year old man volunteers as tribute and you decide to first examine his gastrointestinal system.
"No palmar erythema" you say with confidence, before moving on from the hands. You eventually get to the abdomen and percuss for the liver like a boss. "Spleen not palpable" - you are killing this! After completing the exam by offering a DRE (perhaps a little enthusiastically in retrospect), you dive straight into the cardiovascular examination. "No Janeway lesions or Osler's nodes..." The rare eponymous hand signs are rolling straight off your tongue - Dr Keat must be so impressed! Time to whip out your brand new stethoscope, and what luck - you hear something! "There is a murmur, loudest over the aortic valve". By completion of the examination you are visibly glowing, although slightly confused that Dr Keat doesn't look as awed by your brilliance. "Not bad" he says "But I have a few questions..." Uh oh.
"You mentioned palmar erythema. Why do we check for palmar erythema in a gastrointestinal exam? What sort of conditions might give this finding?" Um...
"And you also mentioned the spleen was not palpable, yes? Tell me how someone with chronic liver disease might end up with a large spleen." Ok, just give me a minute to think...
"You students love mentioning Osler's nodes and Janeway lesions together but I found no one can actually tell the difference. Can you?" Well, Talley just said to mention it...
"And as for your murmur over the aortic valve... You didn't mention if it was systolic or diastolic. Do you know how to tell the difference?" ...Don't I get points for not just saying heart sounds dual no murmur?
Dr Keat has hit you with some humdingers and brought you back to Earth. Luckily, someone has just put in an NoA for conference leave that needs to be unapproved, so you have some time to Google the answers before Dr Keat gets back.
1) What is the physiology of palmar erythema - what are some causes that would allow detection on gastrointestinal exam?
2) How does chronic liver disease cause a palpable spleen?
3) What is the difference between Janeway lesions and Osler nodes?
4) How do you tell the difference between a systolic and diastolic murmur?
Physicians Challenge 16: Good Old TB
You are the intern on the respiratory team. Mrs Vy is a 38-year-old Vietnamese female who presented with chronic productive cough and mild haemoptysis. For the past month, she lost 10kg and had fevers, chills and night sweats. She is a non-smoker and has not had previous exposure to asbestos. On physical examination, she appears to be cachectic, with reduced breath sounds over the right lung apex. Your consultant, Dr Miliari suspects tuberculosis as one of its differential diagnosis. She says to you, “Order the tests for TB”.
1. What are the work-up investigations for TB?
2. The student nurse caring after Mrs Vy asks, “Are there any special instructions with these tests?”
3. It is just your lucky day that your registrar grills you, asking “What are the medications we give for TB?”
1. Work-up investigations for TB
(refer to the flowchart below)
TST = Tuberculosis Skin Test
IGRA = Interferon Gamma Release Assay
2. Special instructions for the tests
3 samples of morning sputum over 3 days-->early morning sputum preferred prior to eating/drink
3. Medications for TB
Depending on pt demographic and comorbidities, it depends which meds are chosen for optimal treatment. The four commonly used anti-tubercular drugs include:
Flow chart from RACGP: http://www.racgp.org.au/afp/2012/july/tuberculosis-testing/
Physicians Challenge 15: She’s Swell
This one's for you, year 1 and 2!
A 76 year old lady presents to ED with progressive shortness of breath on exertion and bilateral pitting pedal oedema. Her son mentions that she has a background history of hypertension, hypercholesterolaemia, gout and hyperthyroidism. Her hypertension has been poorly controlled recently. She is a non-smoker and does not drink alcohol.
1. What is the most likely diagnosis?
2. What is the likely mechanism leading to this presentation? Correlate your mechanism to her symptoms.
3. What symptoms and signs can help differentiate between left and right heart failure?
4. What are the principles of treatment for this patient?
1. What is the most likely diagnosis?
Acute decompensated left heart failure, also resulting in right heart failure.
Note that diastolic heart failure is now referred to as “heart failure with preserved ejection fraction”, and systolic heart failure is referred to as “heart failure with reduced ejection fraction”. Ejection fraction refers to how much blood is pumped out of the left ventricle with each contraction – i.e. a measure of systolic function.
2. What is the likely mechanism leading to this presentation? Correlate your mechanism to her symptoms.
Hypertension (increased systemic vascular resistance) leads to L ventricular hypertrophy and increased preload (left ventricular wall stress at end diastole). Eventually this causes impaired L ventricular filling and increased afterload (can be thought of as L ventricular wall stress during systole), as well as increase the pressure in the L atrium. This increased pressure causes pulmonary venous congestion leading to pulmonary oedema and shortness of breath.
Increased pressure in the pulmonary veins is transmitted to the R ventricle, resulting in increased R atrial pressure. This leads to signs such as elevated JVP, and peripheral venous congestion resulting in peripheral pitting oedema.
3. What symptoms and signs can help differentiate between left and right heart failure?
Left heart failure: dyspnea, orthopnoea, paroxysmal nocturnal dyspnea, crepitations in the lung bases, lateral displacement of apical impulse
Right heart failure: parasternal heave (RVH), sacral oedema, pedal oedema, distended neck veins, elevated JVP (signifies increased R atrial pressure), RUQ pain, hepatomegaly, hepatojugular reflux, ascites, scrotal oedema
4.What are the principles of treatment for this patient?
Adequte oxygenation, restore haemodynamic stability, correct volume overload and prevent complications.
- OXYGEN: monitor SpO2, high flow oxygen therapy via non rebreather mask +/- non-invasive ventilation.
-POSITION: Seated position
-DIURETIC: to correct volume overload, e.g. furosemide (Lasix).
-TREAT HYPERTENSION: early vasodilator therapy is beneficial in severe hypertension, IV nitroglycerin is preferred in the context of acute decompensated heart failure.
- Urine output monitoring (e.g. using a catheter)
- Sodium and fluid restriction
- Venous thromboembolism prophylaxis
Long term for patients with preserved ejection fraction:
- Control associated condition – hypertension
- Control heart rate
- Control of pulmonary congestion and peripheral oedema with diuretics
- Lifestyle measures: fluid restriction, sodium restriction, regular exercise.
Note that patients with heart failure with reduced ejection fraction require differing long term treatment. You can read more about it in the resource listed below.
Treatment of acute decompensated heart failure: Components of therapy. Available from: https://www.uptodate.com.acs.hcn.com.au/…/treatment-of-acut…
Physicians Challenge 14: Everything Derm
For Physician's Challenge 14, we have 14 rashes and skin lesions for you to spot diagnose. Benign, acute, common, severe, chronic, mild, rare and life threatening - its all there for you to test yourself!
ONE ANSWER PER PERSON (to spread the PhysSoc love around - just pick one of the images, A through to N, and comment your diagnosis).
Physicians Challenge 13: Tummy Turns
Tess, a 26-year-old Caucasian female, presents to her GP with a chief complaint of abdominal pain and diarrhoea. Her symptoms began 3 weeks earlier, with the abdominal pain described as intense cramping that is mostly diffuse but seems to be more intense in the right lower quadrant. She also has had nausea, vomiting, fatigue, weakness, and shortness of breath. The diarrhoea occurs approximately 10 times per day is described as watery, non-bloody and containing mucus. Tess has smoked 1 packet of cigarettes daily for the past 5 years and does not drink alcohol.
What is the likely diagnosis? What further tests could be done to confirm this?
Physicians Challenge 12: Mr Lung
Mr Lung--a 67-year-old gentleman presents to you with worsening cough, sputum production and shortness of breath.
He is a smoker of about 1 pack a day for the past 50 years. He recalls having "my normal bad morning cough" for many years; that is productive of yellow sputum at times. Otherwise he feels generally well during the day. He reported that he was in "his normal state" until 2 weeks ago when he developed a flu.
Since then, his cough has worsened considerably with thick sputum production. He is unable to walk more than 20m without stopping to "catch his breath". The picture below is your observation of what Mr Lung is doing during the history and examination.
Why does pursed lip breathing happen in these patients? And what are the pathophysiologic changes in emphysema v.s. chronic bronchitis?
Physicians Challenge 11: Sugar Rush
A 36-year-old woman is evaluated after MVA with LOC. Initial labs show serum glucose of 1.7 mmol/L. The patient recovers consciousness with intravenous dextrose. Head CT is negative. On interview, she reports LOC occurred before her accident. She relates recurrent episodes of sweatiness, tingling and confusion occurring with increasing frequency over the last year. The episodes improve with eating. She is admitted for observation and 4 hours later is found by her nurse to be irritable and confused. You order a serum glucose level and other labs.
1. Describe Whipple’s triad?
2. List 3 more common causes of hypoglycaemia
Physicians Challenge 10: Bloody case
A 71-year-old male is referred to the ED by his family doctor following a two-month history of worsening fatigue, shortness of breath and fevers. He denies rigors, chills headache, has no cough and is otherwise well. His past medical history is significant for ischaemic heart disease (MI 6 years ago) for which he takes aspirin 100mg, GTN as required and metoprolol 5mg. He also takes Panadol Osteo for arthritis in his knees. There are no reported allergies, no smoking history and only moderate alcohol intake. He returned from a holiday in Cambodia 3 months ago.
On examination, his temperature is 38, heart rate is 98 and regular and respiratory rate is 20. There is no evidence of jaundice but some bruises are noted and there is a diffuse, non-specific rash on his torso and proximal limbs. Cardiorespiratory exam is unremarkable and gastrointestinal examination reveals hepatosplenomegaly.
You order the following tests:
Hb: 82 (135-180)
WCC: 16 (4-11)
Plts: 90 (150-400)
MCV: 90 (80-100)
Neutrophils: 1.2 (2-7.5)
His LFTs and iron studies are within the normal ranges. You also send off some blood cultures and a Quantiferon Gold test. A CXR is performed with the results shown below. Thick and thin blood films are also performed with the thin film shown below. The gram stain on the blood cultures comes back a few hours later and is reported as “No organisms seen".
What is the likely diagnosis and what is the key supporting piece of information? How would you confirm the diagnosis?
Physicians Challenge 9: Confused
You are a third year medical student on your General Medical term and are called by the orthopaedic surgeon for a consult. The patient is a 61 year old lady who underwent an uncomplicated, elective total hip replacement yesterday and has now become acutely confused.
A comprehensive medical history is difficult to attain given her confusion, but with the help of the nurse and the patient in the adjacent bed you work out that the patient had been very well post-operatively but became agitated and disoriented in the early hours of the morning.
On examination you find her temperature is mildly elevated (37.6). The surgical site is clear and her abdomen is soft and non tender, with the liver edge felt about 4cm below the costal margin. Cardiorespiratory exam seems normal. You do an MMSE and she scores 22/30, with most difficulty in orientation to time and place and with serial 7s. You also notice she has an IV drip and IDC in, both of which seem to be working well.
You go to review the admission notes for her medical history which is significant for chronic alcoholic liver disease, hypertension, GORD and polymyalgia rheumatica - for which she takes perindopril, indapamide, ranitidine and regular paracetamol. She has also been charted for oxycodone by the anaesthetist to manage postoperative pain and is on IV cefazolin.
What is the likely diagnosis in this lady? How will you advise the surgeon to manage her?
This case was an example of a very common case in the hospital - acute delirium. Delirium is characterised by an acute onset, fluctuating course of decreased or disturbed consciousness. There are 3 main types: hyperactive, hypoactive and mixed.
Inattention is one of the key signs to look for in delirium, and it helps differentiate from patients with dementia. On MMSE, this manifests as difficulty with serial 7s or backwards spelling WORLD. Other things to look for include disorientation to time and place, poor short term memory, poor sleeping habits and disordered thinking.
Anyone who has one a general medicine or geriatrics term will be able to tell you that there are lots of causes (common and rare) for delirium - and any number of them could be implicated in the case of our lady. One useful acronym to remember the causes is I WATCH DEATH, or DELIRIUM - find one that works for you. In this case, the causes important to consider include pain, alcohol withdrawal (an important one - easy to miss but also easy to prevent!!), constipation from narcotics, actual side effect of narcotics or anaesthetic, AKI, polypharmacy, even stroke.
Investigation may include bloods, septic screen (urine dipstick, CXR and blood cultures), LP, ECG, EEG and other imaging. Management is based on identification and treatment of the underlying cause. Additional supportive measures such as reducing stress, minimizing medication (and particularly avoiding anti-psychotics where possible) and removing physical constraints such as catheters are also important - in this case though, the IDC is necessary!
Physicians Challenge 8: I Had A Bit Too Much To Drink
Your ICM mentor decides to take you to the emergency department to see a new patient, an 83 year old female who presented this morning complaining of nausea, epigastric pain and shortness of breath for the last 2 days. Your careful questioning elicits a history significant for chronic alcohol abuse which started shortly after her husband passed away 15 years ago. She admits to regularly drinking half a bottle of port and a bottle of red wine each day. In the last 5 days, she has been drinking more, and hasn't been eating her meals, however in the last 48 hours she stopped drinking due to her nausea and vomiting.
Your ICM mentor demonstrates a gastrointestinal examination to your group, which is significant for tachycardia (105, regular), tachypnoea (RR 22), epigastric tenderness and evidence of dehydration. You then have a look at her investigation results on admission:
Sodium 142 mmol/L
Potassium 4.8 mmol/L
Chloride 101 mmol/L
Anion gap 35
Glucose 4 mmol/L
Blood alcohol level 0
arterial pH 7.14
Serum acetone concentration 16.8 mmol/L
Serum lactate 2.3 mmol/L
Amylase 954 U/L
Lipase, 210 U/L.
Urinalysis: Ketones present
ECG: no acute ischaemic changes
What is your provisional diagnosis? How does this explain her investigation results? Your answer should explain the mechanism leading to her current condition.
What are your next steps in management?
Image source: http://www.mac.sa.gov.au/campaigns/drink-driving
This case demonstrated an acute presentation of alcoholic ketoacidosis (AKA) precipitated by an alcohol binge and poor nutrition, onset of vomiting and abrupt cessation of alcohol intake.
The patient's nausea, vomiting, epigastric pain and elevated serum amylase and lipase indicate acute pancreatitis as the underlying cause. Persistent vomiting and alcohol cessation in this context are key causes of her ketoacidosis.
Here is some key information which explains how this condition developed:
What is ketoacidosis?
Ketoacidosis results from accumulation of ketone bodies in the blood, resulting in metabolic acidosis. Ketone bodies include acetoacetate, beta-hydroxybutyric acid (usually the main cause of ketoacidosis, produced when acetoacetate is reduced by NADH) and acetone.
AKA accounts for 20% of cases of ketoacidosis.
What clinical features make you think of alcoholic ketoacidosis (AKA)?
AKA is likely in alcoholic patients with a history of recent binge drinking with an abrupt cessation, often due to alcohol related complications, such as pancreatitis, gastritis, hepatitis or pneumonia. Common features in these patients are minimal caloric intake, abdominal pain and persistent vomiting. They usually think quite clearly and are able to provide a complete history.
Blood alcohol levels may be 0, and patients do not have glycosuria.
How did AKA develop in this patient?
Dehydration, impaired insulin effects and hormonal responses cause accumulation of ketone bodies.
Vomiting, acute starvation and cessation of alcohol intake cause an increase in catecholamines and cortisol in the body, as well as a decrease in insulin and increase in glucagon (due to fasting state). This, along with the alcohol binge, leads to an increase in lipolysis, reduced glycogen storage and increased production of ketone bodies.
Alcohol is metabolized in the liver, oxidised to acetalydehyde and then to acetic acid. This involves conversion of NAD+ to NADH. This shift to NADH causes:
- Suppression of gluconeogenesis
- Acetic acid is reduced to beta-hydroxybutyric acid – a ketone body. (important in diagnosis of AKA)
The patient has been vomiting, resulting in fluid depletion and reduced renal output – less ketone bodies are renally excreted. This results in accumulation of ketone bodies in an increasingly dehydrated and unwell patient.
Refer to the flowchart for more details.
Correct volume depletion, glycogen depletion and elevated NADH/NAD+ ratio. IV fluids and glucose are highly effective and resolution in uncomplicated patients can occur in 6-8 hours.
Unless the patient is hyperglycaemic, mainstays of treatment are:
- IV fluids – 0.9% saline solution – this is important in both acute pancreatitis and AKA
- IV thiamine (100mg) – prophylaxis against Wernicke encephalopathy
- IV 5% dextrose – stimulates NADH oxidation, replaces glycogen stores, increases insulin:glucagon ratio
- Antiemetics, analgesia – as part of initial treatment of acute pancreatitis
1. Ngatchu T, Sangwaiya A, Dabiri A, Dhar A, McNeil I, Arnold J. Alcoholic ketoacidosis with multiple complications: a case report. Emergency Medicine Journal. 2007;24(11):776-777.
2. IMAGE SOURCE: Carpenter C. Alcoholic Ketoacidosis. In: Adams J, ed. by. Emergency Medicine [Internet]. 2nd ed. Saunders; 2013. Available from: https://www-clinicalkey-com-au.ezproxy.uws.edu.au/…
3. Mehta A, Emmett M. Fasting ketosis and alcoholic ketoacidosis [Internet]. UpToDate. 2016. Available from: https://www.uptodate.com/…/fasting-ketosis-and-alcoholic-ke…
Physicians Challenge 7: I’m Bloody Tired
A 48 year old male has become progressively more fatigued at the end of the day. This has been going on for months. In the past month he has noted paresthesias with numbness in his feet. A FBC demonstrates the findings shown.
A peripheral blood smear shows red blood cells displaying macro-ovalocytosis and neutrophils with hypersegmentation.
What is the diagnosis from these findings? How do you explain the neurological findings?
Physicians Challenge 6: I’m Getting a Bigger Tummy
A 39 year old gentlemen presents with a 5 day history of worsening abdominal distension associated with generalised abdominal pain and has been febrile for the past 2 days.
He has also had some episodes of vomiting and some loose bowel motions but saw no blood. His past medical history is significant for cirrhosis of the liver and he has has previous hospitalisations for hepatic encephalopathy. His social history is significant for chronic alcohol abuse.
On examination, the patient is febrile, mildly tachycardic and mildly dyspnoeic. His abdomen is distended, tender and tense to palpation. He also has shifting dullness.
What are the primary diagnostic investigations in this patient? What is the likely diagnosis and how would you confirm this?
Physicians Challenge 5: I’m All Blocked Up!
Mr Bowl is a 70-year-old man on the orthopaedic ward. 5 days ago, he had a hemiarthroplasty of his left hip. He was recovering well until the development of abdominal distension recently. In the last 3 days, he has not opened his bowels and has not passed flatus. His medical history is significant for an appendectomy 45 years ago.
Examination revealed significant distended abdomen with mild generalised tenderness. Abdomen was resonant to percussion, with some bowel sounds heard. There are no hernias; with DRE revealing an empty rectum.
An X-ray of the abdomen was performed and shown below.
Which type of obstruction is seen on the AXR and what clues indicate so? Based on all the information above, what is the most likely diagnosis?
Large bowel obstruction--the AXR shows the dilated transverse colon--with presence of haustra (folds that do not fully cross the bowel lumen).
The most likely diagnosis based on the history, examination and investigation is pseudo-obstruction (when there is no mechanical causes found). It is important to remember that cause of LBO is hard to determine through AXR itself.
Pseudo-obstruction occurs in patients post trauma, infection, or surgery. Systemic causes include sepsis, metabolic disturbances and drugs. Conservative treatment involves keeping patient NBM, IV fluids and NG decompression. Decompression can also be done through colonoscopy.
Physicians Challenge 4: I’m Turning Yellow
70 year old African male presents with jaundice, anorexia and weight loss for 2 months. He describes yellow eyes and skin, dark urine and pale stools. Denies abdo pain, nausea, vomiting, diarrhoea, constipation, recent travel. Non smoker and social drinker of alcohol. On abdominal examination, a firm, non-tender smooth mass extending 4 cm below the right costal margin was felt, dull to percussion. No peripheral stigmata of chronic liver disease.
What is the type of jaundice described here? What is the textbook clinical sign and hence most likely diagnosis?
Obstructive jaundice due to the dark urine and pale stools. The dark urine is due to conjugated bilirubin binding less tightly to albumin in obstructive jaundice causing it to be excreted in the urine, giving it a dark tea colour. In addition, bile duct obstruction prevents the excretion of bilirubin into the intestines. This in turn results in stools not accumulating the bile pigments which normally make it dark in colour, resulting in pale stools.
The textbook clinical signs is Courvoisier’s sign which refers to painless jaundice with a palpable gallbladder indicating that the cause is most likely not a gallstone, but more likely to be due to pancreatic malignancy. This is due to the fact gallstones are normally formed over an extended period of time causing a shrunken, fibrotic gall bladder which does not distend easily and is hence not likely to be palpable.
Physicians Challenge 3: ECG & Palpitations
A 20-year old medical student complains of palpitations. The attacks occur about once per year. They start suddenly, his heart feels very fast and regular, and he quickly feels breathless and faint. The attacks then stop suddenly after a few minutes. Examination is normal and here is his ECG. What does his ECG show and what treatment should he have?
Wolff-Parkinson White (WPW) syndrome Type A, requiring treatment for the ablation of the aberrant conducting pathway.
The ECG shows:
-Short PR interval (112ms)
-QRS complexes are a little wide (124ms)
-Slurred upstroke of QRS (delta wave) - This is characteristic of WPW!
-Dominant R wave in lead V1
-Widespread T wave inversion
There is resemblance to an ECG of RV hypertrophy, because this is type A with left-sided accessory pathway.
Source: Hampton JR. 150 ECG Problems. 2nd edition. London: Elsevier Science Limited, 2003: 29-30.
Physicians Challenge 2: Car Crash
A 22 year old male is brought in to the Emergency Department after a high speed motor vehicle accident with suspected spinal cord injury. You examine him and find that he has lost all sensation in his lower limbs, trunk and the majority of his upper limbs, with some sensation preserved in the lateral areas of his arm proximal to the elbows bilaterally. He is unable to move his arms and legs except for some weak shoulder abduction.
What is the level and degree of his spinal cord injury? How could you confirm this?
Transection of the spinal cord below the level of C5 manifests itself as a quadriplegia. The presence of sensory and motor impairment on both sides of his body suggest that the cord damage is bilateral and affecting both the dorsal column sensory pathways and the motor pathways. The preservation of sensation in his lateral arms suggests that C5 is still in tact, and thus the damage is likely just below this. Good news for his breathing (remember - C3, 4, 5 keep the diaphragm alive)!
Neurological injuries present a good opportunity to make clinical diagnosis, as the signs are often well elicited on clinical examination. In this patient, we see compromise to his sensation and muscle strength. Other signs you may expect are loss of anal tone, hyporeflexia acutely, with the development of hyperreflexia and spastic rigidity after a few days or weeks, and changes to heart rate and blood pressure if the sympathetic and parasympathetic chains are affected. Otherwise, investigation with MRI or CT can help localise the level and extent of the damage, as well as pick up any other injuries from the trauma that are not yet clinically apparent.
Physicians Challenge 1: MRI
A 64 year old female presents to the hospital (A), and 3 days later her MRI scan reveals the lesion in (B). What is the likely diagnosis?
NOTE: the lesion is indicated by the yellow arrow.
Transient Global Amnesia may be confirmed by punctate lesions in the hippocampi (MRI brain) as shown in the images. Patients present with both anterograde amnesia (inability to form new memories) and retrograde amnesia (inability to recall previously stored memories). These symptoms occur within minutes or hours, and can be precipitated by excessive activity, emotional stress, headache, nausea or vomiting.
The impairment of memory gradually resolves (usually in 24 hours) and this can be measured using serial verbal recall tests. When the lesion (shown in the images) is present in MRI, this may be indicative of a small localised stroke.
Image obtained from Yang et al. with permission. Source: Yang Y, Kim S, Kim J. Ischemic Evidence of Transient Global Amnesia: Location of the Lesion in the Hippocampus. J Clin Neurol. 2008;4(2):59. (Figure 1)