History Revisited With Examination ! It CAN be better than a CT scan!

Dear Bloggers

A 70 year old patient was recently admitted with fever of 'unknown' origin to a rural hospital.

The patient had developed the fever suddenly with associated shivering sensation and had presented to the same hospital. Other symptoms included some rhinorrhoea and a mild cough. The on-call physician took blood cultures and prescribed an antibiotic for an URT infection and the patient went home at her own request.

However, after several days the blood cultures grew Group G Streptococcus in both sets of culture bottles. The patient was contacted and admission was arranged for inpatient investigation and treatment.

The patient had a background history of suspected infective endocarditis 6 months previously with the same type of organism, which was treated accordingly. However, at that time the transthoracic and transesophageal echocardiograms were normal. Colonoscopy revealed several polyps but no source of bacterial translocation was identifiable.

The patient was treated for suspected I.E and made a good recovery at that time.

Otherwise, there was no other apparent medical history.

The patient was taking no regular medications.

Alcohol consumption was moderate with several cups of Japanese sake per day and the patient smoked several cigarettes per day for the last 30 years.

Of note, she had recently bought a puppy.

Physical Examination had failed to establish the focus of the fever.

The laboratory data revealed a raised white cell count, raised inflammatory markers, and mild elevations in the liver function tests only.

The chest radiograph was within normal limits.

Transthoracic echo revealed previously noted mild valvular insufficiencies but there was no worsening and no vegetation to be seen.

A CT scan was performed to look for an abscess but only some mild splenomegaly was identified. The CT was hence, quite unhelpful.

At this point, the suspected diagnosis was vegetation negative endocarditis. However, if one reviews the Modified Duke's Criteria, this patient does not meet the criteria for definite I.E. with only one major criteria (typical bacteria) and two minor criteria (Fever>38 degrees and underlying valvular heart disease).

On reviewing the patient, several additional questions were asked:

• The patient had previous tooth problems and the bottom left incisor was loose but no dental treatment had been performed recently
  
• The patient had experienced several flea bites recently from her dog
  
• There was no history of sinusitis or headaches
• The patient had been diagnosed with a type of eczema for which ointment had been prescribed but the patient could not remember the name of the therapy
  
• There was no foreign travel
• No history of consumption of raw or under cooked food stuffs
  

On re-examination, new information came to light as follows:

HEENT- eczematous changes of the upper eyelids and eyebrows consistent with seborrheic dermatitis. Scalp examination also revealed seborrheic dermatitis (fungal origin). No sinus pain. Loose front, lower incisor (when pushed with a chopstick at the bedside) but no acute gingivitis seen.

CVS: pulse 80 regular, BP 120/80mmHg, JVP not elevated. Heart sounds I + II. No III/IV sounds. Pansystolic murmur at the apex radiating to the left axilla - Levine II/VI. Murmur loudest on expiration. No carotid bruits. No peripheral stigmata of I.E.

RESP: RR 14/min, Sats 98% on room air, trachea central and no tug. Percussion resonant and no crackles or wheeze.

ABDO: Soft, non-tender, no masses, no clinical hepatosplenomegaly on palpation but dullness in Traub's space. Small, non-tender, lymph nodes in the groin areas.

Skin: Several healing flea bites on the abdomen. Redness and increased temperature of the left hand after failed insertion of a venous line on the admission day. As noted above, eczematous changes over the face. Her left leg revealed a well circumscribed area 3 x 3 cm with peripheral redness with central clearing consistent with fungal infection. Foot examination revealed extensive tinea pedis (fungal infection).

The extremities had not been mentioned during the original presentation of the history. It therefore came as a surprise to see a 30cm vertical anterior scar running down the right tibia with extensive erythema of the skin with soft tissue swelling. The patient admitted to a previous fracture of the tibia.

On noting the leg changes, further questioning revealed that the redness and swelling had got worse over the last 10 days but it was not painful and so the patient did not mention it especially as it was a chronic problem for which she thought her current fever was unconnected. The patient admitted that several months earlier there had been a flare-up which required antibiotic therapy. Examination of the leg revealed increased temperature of the lower limb and tapping the bone was non-painful. These changes were clearly acute on chronic but raised the possibilities of cellulitis +/- chronic osteomyelitis.

Group G streoptococcus is an uncommon cause of cellulitis but this patient had the risk factor of previous injury and extensive fungal skin infection which can allow entry of skin associated bacteria. Moreover, Group G strep is also an uncommon cause of osteomyelitis (please see Medline).

The fact that the same organism was identified 6 months previously when the diagnosis was 'endocarditis' and that several echocardiograms showed no vegetation, makes I.E. unlikely and recurrent cellulitis / chronic osteomyelitis of the right leg far more likely a cause.

The patient was commenced on benzylpenicillin for which the bacteria was sensitive and an MRI was considered to look for osteomyelitis.

Take Home Message

• Patients do not always tell you the history you want to hear to make a diagnosis. You have to ask the right questions! Then the history comes forth from the patient bit by bit.

• If you see a skin abnormality or a bony abnormality, ASK about it. 'What happened here?' In this case, the patient had chronic problems with the leg dating back 40 years and the patient did not think that it was relevant. But it is the physician's duty to recognise the problem to decide if it is relevant. Hence, using history and physical examination to establish the facts.

• If the history, physical, lab data and echocardiograms do fit the picture for I.E. then don't diagnose I.E. Use the Modified Duke's criteria, but if the criteria are not met, then I.E cannot be made as the diagnosis. Consider other causes of chronic infection e.g. sinusitis, osteomyelitis, abscess....

• Examine your patients from HANDS to HEAD to TOE and look actively for problems that might otherwise account for the fever and bacteraemia despite the 'lack of symptoms'. Do not just accept that because the patient 'did not say , that they therefore do not have'. ASK and you will KNOW.

• This is the importance of using the Review of Systems (ROS) questions to probe each system for problems. More focused questions can then be asked if clear abnormalities come to light. Without using the ROS you will miss important problems that could lead you to the diagnosis. ROS is like a verbal CT scan -- it is used to 'scan' each system with trigger questions that make the doctor consider various diagnoses if the patient says 'yes' to such questions. Indeed, it takes longer than a CT scan to perform but is more localising and without radiation. **Always remember that by subjecting your patient to a CT scan you increase their risk of malignancy and so CT should be avoided if at all possible**
  

• In this case, a good old fashioned history and physical examination made the diagnosis at the bedside rather than a barrage of blood tests, echocardiograms and a 'pan-man' CT. If the diagnosis does not seem right then it probably is not right, and as such, please go back to the patient and re-interview and re-examine to get more relevant information. The answer is sometimes staring you in the face!
  

Have a great weekend.

August 2009 Case

Dear Bloggers

Here is August's case. It is a great one for sure! Please have a go and see if you can get the diagnosis!

A 65 year old lady was admitted to the hospital with loss of consciousness.

She had been found by her husband having collapsed in the toilet at 3am. The loss of consciousness had been unwitnessed but the patient was found to have urinary incontinence. Her husband called for an ambulance and she was transferred to the ER department. There was no obvious head trauma and no tongue biting.

The patient later became rousable in hospital and admitted to feeling dizzy when standing over the last few days. The patient also had some loose stools over the preceding days prior to admission but she described the colour as normal. There had been no associated abdominal pains. She denied straining whilst defecating.

She also admitted to recent ‘pins and needles’ in her left arm and some double vision over the preceding days prior to admission. She had no perioral paraesthesia.The symptoms had come on gradually and nothing had made them better or worse.


She denied the following symptoms

• CVS: No chest pains, no palpitations, no leg swelling
• RESP: No cough, bo sputum, no breathlessness
• ABDO: No nausea, novomiting, no haematemesis, no malaena, no swelling, no jaundice.
• Musc: No muscle pains, no weakness, no joint problems.
• URO: No frequency, no nocturia, no haematuria.
• CNS/PNS : No headaches, no visual loss, no speech disturbance, no hearing loss. No weakness of arms or legs. No unsteadiness.
• Endo: No excessive thirst, no tremor, no sweats, no weight loss
• Skin: no skin problems

Previous Medical History

• Right adrenal tumour – diagnosed 5 years ago. The patient had undergone unilateral adrenalectomy but she was uncertain of the final diagnosis.
• Hypertension
• Constipation
• Paroxysmal Atrial Fibrillation (PAF)
• Hyperuricaemia


Medications

• Disopyramide 40mg 4x/day
• Aspirin 81mg/day 1x/day
• Allopurinol 100mg/day 1x/day
• Voltarol 50mg 3x/day
• Ranitidine 150mg 2x/day
• Lactulose 10ml 2x/day
• Senna two tablets 1x/day

No Known Drug Allergies

Family & Social histories: these were uncertain on the admission day

On Examination

General: Patient was alert. GCS 15/15 and was oriented in time, place and person. Afebrile.

No JCCO; conjunctival pallor (+), rubbery, mobile, smooth lymph nodes (+) in the left and right axillae. Maximum diameter of the LNs approx. 15mm.

HEENT: No evidence of fracture or soft tissue injury. Tongue was atraumatic. Mouth did not demonstrate any blood. Ears - no blood or fluid. Nose - no blood or fluid.

CVS: Pulse 110 / min, regular. BP 86/70mmHg. JVP not elevated. No heaves or thrills. Apex in normal position. Heart sounds 1 + 2 normal. No S3 or S4. No murmurs. No leg edema or signs of calf swelling / pain / redness.

RESP: RR 16/min, SpO2 95% on room air. Trachea was central. Percussion note was resonant. Auscaltation revealed normal vesicular breath sounds.

ABDO: Soft, non-tender, no masses, no hepatosplenomegaly, no inguinal lymphadenopathy. No bladder distension, and no renal angle tenderness. Rectal exam – black stool.

Musculoskeletal: No focal abnormalities

CNS

II: grossly normal visual fields. Pupils equal and reactive to light and accommodation + consensual response. Proptosis of the left eye.

III/IV/VI: impaired abduction of the left eye with associated double vision when looking to the left lateral side. Other eye movements were all normal.

V: Normal motor and sensory components

VII / VIII /IX / X / XI / XII: all grossly normal.

PNS

Tone – normal throughout the upper and lower limbs

Power – Upper and lower limb power 5/5 throughout

Reflexes

RUL LUL RLL LLL
Supin +/- ++ +/- +/-
Biceps +/- ++ +/- +/-
Tricep +/- ++ +/- +/-
Knee +/- +/- +/- +/-
Ankle +/- +/- +/- +/-

Sensory: Gross sensation , nociception and joint position senses appeared intact.

Coordination: No cerebellar signs

Fundoscopy was not performed.

Endocrine: no tremor, no thyroid enlargement, no evidence of bitemporal hemianopia.

Skin: no focal abnormality

Question 1: From the history and examination, please make an appropriate problem list.

Question 2: Please provide a differential diagnosis (es).

Question 3: What would you immediately do for this patient?

Question 4: What tests would you perform and why?

Question 5: What other bedside physical examination test(s) could provide additional information to aid your diagnosis?

July's Case 2009- The Answers

Dear Bloggers

I hope that you found this case thought provoking.

Professor Masami Matsumura has kindly considered this month's case despite his busy schedule. I thank him for his time and input.

His answers to the blog case are as follows:

Thank you for showing difficult case again. I would try to solve.

The patient was a 64-year-old lady.

Problem list on admission

#1Benzodiazepine overdose

Diazepam 1,000mg and Lorazepam 200 mg

Altered mental status, GCS 3/15

Tone decreased throughout

Reflexes generally depressed

No response to pain

#2Aspiration pneumonia

Fever

Tachycardia

High RR [respiratory rate]

Hypoxia

#3History of anxiety and insomnia

Problem list on second episode

#1 Unresponsive

#2 Shock

#3 Hypoxia

#4 Acidemia, respiratory acidosis

#5 Tachycardia

#6 After flumazenil administration

Question 1: Why did the patient lapse into unconscious despite initial improvement on the evening of admission to the hospital?

Benzodiazepine overdose will last for several days and flumazenil is a short-acting drug. I think second episode was caused by benzodiazepine overdose again.

Question 2: Why did the patient deteriorate so quickly during resuscitation, with profound hypotension and sinus tachycardia >200/min and why did it resolve?

PSVT with high rate can cause hypotension. Additional flumazenil administration and intubation can alleviate patient condition better.

Question 3: What acid-base disturbance is demonstrated by the blood gas?

Hypoxia and respiratory acidosis with hypercapnea caused by benzodiazepine overdose.

Question 4: What additional therapies may have helped this patient when admitted to the hospital that could have been commenced in the ER department?

Activated carbon administration can absorb overdose of benzodiazepine in GI tract.

What had happened in this case? (Question 1-3 are covered in the following text)

Firstly, we must look at the drugs. This patient has both long and short acting benzodiazepines. Remember that benzodiazepines get metabolised into other active benzodiazepines that can have longer half-lives. Hence, these drugs can have sedative effects for a prolonged period of time. The effects are more marked in the elderly who have reduced ability to excrete these drugs. For example, diazepam has a half-life of 20-40 hours but its active metabolite is Nordazepam which has a half-life of 60 hours!! The overall duration of action is about 24-48 hours !

Nordazepam is converted to Oxazepam (the same compound produced from Temazepam) which is then combined with glucuronic acid and excreted renaly. On the other hand, Lorazepam is a shorter acting benzodiazepine although is half life is 8-12 hours. However, it has no active metabolite so its overall half is the same.

The action of Flumazenil is rapid and hence it is no surprise that the admitting resident considered the patient 'stable' after injecting the 'antidote'. However, Flumazenil only acts for a short period of time (maximum of 2 hours) and the actions of the long acting benzodiazepines can return. This is indeed what happened here.

The benzodiazepines caused unconsciousness and respiratory compromise despite the respiratory rate of 24 per minute. The patient had decreased air entry on examination and hypopnea despite tachypnoea. This resulted in CO2 retention and acute respiratory acidosis.

However, if one looks at the ABG result, the HCO3 level is minimally elevated and base excess is -5. These suggest an added metabolic acidosis. This is unsurprising in the presence of severe hypoxaemia. Her calculated bicarbonate should have been 36.2 if a pure respiratory acidosis were present.

The history, physical exam and vital signs suggested that she had SIRS (systemic inflammatory response syndrome) as part of a septic syndrome. The fact that her blood pressure dropped on minimal incline suggested hypovolaemia and / or septic shock.

The patient having vomited and aspirated was evidence enough of an unsafe airway and the patient should have been intubated on admission prior to administration of Flumazenil. Moreover, such patients need to have activated charcoal. Most texts suggest that the activated charcoal be given within 1 hour of an overdose. This is not entirely accurate because some drugs have a slower absorption e.g. Lorazepam, and the use of charcoal can have benefits even after 1 hour. Moreover, in view of the unconscious state, the charcoal could only have been administered with the patient being intubated to protect the airway.


Why did this patient drop her blood pressure and develop a rapid tachycardia?

The side effects of Flumazenil include hypotension and dysrrhythmia aside from the other serious side effect of seizures in patients taking benzodiazepines chronically. In essence, too much Flumazenil had been administered.

Typical guidance suggests starting with 0.2mg then waiting 30 seconds for a response. Following that give 0.3mg and wait another 30 seconds for a response. Following that, 0.5mg can be administered.

Patients may sometimes require Flumazenil every 20 minutes in view of the short half life of the drug especially when long acting benzodiazepines have been taken in overdose. However, this depends entirely on how the patient responds to treatment. Hence, in view of the short lived hypotension and tachycardia, it is likely that Flumazenil being given at too high a dose was to blame here.

Question 4: What additional therapies may have helped this patient when admitted to the hospital that could have been commenced in the ER department?

• Patients should receive activated charcoal even after 1 hour post-overdose and further doses can be administered several hours later if considered appropriate.
• If the patient has a GCS of less than 8/15, intubation should be initiated to protect the airway and also to allow for activated charcoal to be administered. Remember though, an ET tube is not completely 100% protective against aspiration. Also remember the saying -- 'if the GCS is less than 8 then intubate'
• Flumazenil should be used with extreme caution because of its adverse side effects and should be given in low dose and titrated up. Despite the ability to reverse the effects of the benzodiazepines, its actions are short lived and repeated doses may be necessary. Remember though, benzodiazepines do not usually cause significant respiratory depression making them relatively safe in overdose. Most patients just sleep off the effects of this class of drug. It is when respiratory depression occurs then the antidote should be considered and especially when taken in combination with other CNS depressants.
  
• Remember that Flumazenil is CONTRAINDICATED in mixed overdoses with Tricyclic Antidepressants as the effects of the latter drug can be increased.
• Patients with sepsis often require large amounts of fluid. It is appropriate to administer adequate amounts of fluid and for BP and Pulse to be checked regularly in addition to urine output to assess volume status. In reality, in patient with sepsis, it is better to place a central venous line to assess volume requirements rather than guessing. A CVP of 8-12 cmH20 would be considered an appropriate goal to achieve in sepsis.
  

Take Home Message

The moral of the story here is that we should not be complacent that this is just 'another overdose patient'. If we do not take precautions and manage such patients appropriately, then problems can and do occur to the detriment of the patient.

In cases of overdose, the patient should be managed as a minimum in a high-intensity emergency medicine admissions unit with experienced staff or on an HCU or ITU . Full monitoring equipment should be utilised. Patients should not been placed on a general ward in a side room.

Physicians need to take more care to find out the mental state of the patient before prescribing medications that can be used in overdose and they should not be given out like candy. A thorough drug history is required to be taken by the doctor and drug-drug interactions need to be considered before adding in another medication.

Drug-drug interactions can be easily checked with PDA software e.g. ePocrates

Many thanks to Prof Matsumura.

July's Case: A Patient with Benzodiazepine Overdose

Dear Bloggers

Here is an anonymised case of a female patient admitted to a hospital with an overdose of prescription tablets.

She was a 64 year old lady who had a history of anxiety and insomnia who was normally treated with benzodiazepine therapy on a long term basis. She had otherwise been well. Several days before admission, the patient had been informed of the sudden death of her mother, the news of which she took badly. She lived alone and her main contact was her brother who visited daily.

On the morning of admission, the patient was found by her brother lying on the floor in an unrousable state with vomit dripping from her mouth. Mixed with the vomit were semi-digested tablets. The brother noticed that several blister packs of tablets were empty despite the prescription for the tablets having been given just a few days before.

The brother phoned for the emergency services. On arrival, the emergency personnel checked the Airway, Breathing and Circulation and transferred the patient to the ER department for further assessment and treatment.

The patient had no other significant history.

There was no significant family history and the patient was a non-smoker and non-drinker.

Medications taken in overdose included:

• Diazepam 20mg x 50
• Lorazepam 5mg x 40

ER Vital Signs

GCS 3/15, T 38.6 deg C, Pulse 120 bpm regular, BP125/80mmHg, RR= 24/min, SpO2 92% on 5 L oxygen

Airway - Slight vomit but no obstruction. Cleared with suction.

Breathing - Chest movement equal and normal expansion. Air entry decreased and bilateral coarse crackles with bronchial breath sounds. Oxygen given via face mask.

Circulation - Pulses present, warm peripheries. No evidence of haemorrhage. IV lines inserted and fluid commenced.

Secondary Examination

HEENT - No focal abnormality

CVS - Peripheries warm, pulse 120/min regular and normal pulse volume. JVP not visible. Heart sounds I + II. No III or IV heart sounds. No murmurs. No leg swelling.

RESP - Trachea central and no deviation. No tracheal tug. Percussion anteriorly resonant. Posterior, dullness at both bases. Auscultation revealed coarse crackles and bronchial breath sounds.

ABDO - Soft and non-tender. No rebound or guarding. No masses or organomegaly. Bowel sounds present. Rectal examination revealed no blood and no masses.

CNS - Pupils small but equal and reactive to light. Corneal reflexes positive bilaterally. No facial palsy.

PNS - Tone decreased throughout. Unable to assess power. Reflexes generally depressed. Babinski's unresponsive. No response to pain.

Tests

• The patient underwent an emergency drug screen which revealed only benzodiazepines. No alcohol was present.
• CXR revealed infiltration of the lung in the right lower zone. There was a small pleural effusion present on the left lower zone.
• ECG showed a sinus tachycardia of 125 bpm and no acute changes.
• Other blood tests were otherwise unremarkable except for a neutrophilia.
• Gram stain of tracheal aspirates revealed mixed organisms.

The patient was considered to have a benzodiazepine overdose and aspiration pneumonia.

Treatment - The patient was given emergency treatment with Flumazenil which improved her conscious level whereby she was able to converse with the medical staff. She was commenced on Augmentin intravenously after blood cultures having been taken.

The patient was moved to a private room to await the morning round by the Attending Physician.

In the morning, despite the history of improvement noted by the resident the night before, on arriving in the patients room, she was unresponsive and oxygen saturation had dropped to 75% on oxygen 5L.

Resuscitation was commenced as follows:

• High flow oxygen 15L via reservoir mask
• Blood pressure - 90/60 at 30 degrees incline, 125/75 mmHg lying supine
• IV fluid - high flow, stat
• Flumazenil 0.5mg IV push
  
• ABG - pH 7.02, pCO2 145mmHg, pO2 60mmHg, HCO3 26.4, BE -5
  
• The patient was moved from a side room to the HCU within minutes
• Patient was intubated and commenced on a mechanical ventilation

However, the patient developed profound hypotension of 60/40mmHg and a sinus tachycardia of 200 bpm, the latter as confirmed by 12 Lead ECG prior to tracheal intubation, and both which were initially refractory to high volume fluid administration.

The ECG showed no acute ST changes or T wave abnormalities.

After several litres of fluid the blood pressure increased to 80/50mmHg. Her circulation required minimal support with dopamine to increase the systolic pressure to over 100mmHg. Her pulse dropped back to 125 bpm within 30 minutes of this profound deterioration. The patient was miraculously alert with spontaneous eye opening and nodding in response to verbal commands. The dopamine was later discontinued.

She went on to make an excellent recovery!

Question 1: Why did the patient lapse into unconscious despite initial improvement on the evening of admission to the hospital?

Question 2: Why did the patient deteriorate so quickly during resuscitation, with profound hypotension and sinus tachycardia >200/min and why did it resolve?

Question 3: What acid-base disturbance is demonstrated by the blood gas?

Question 4: What additional therapies may have helped this patient when admitted to the hospital that could have been commenced in the ER department?

Answer To June 2009 Case

Dear Bloggers

Welcome back. Today I will discuss the answer to the recent case. This was one of the most difficult cases I have ever experienced and I thought it would be nice to share this with you all. I was reminded by a colleague also involved with the case, that the rash was in fact painful rather than painless and hence, the initial description of her symptoms was inaccurate for which I apologise :-o

Professor Matsumura has kindly provided his opinion on the case (see below) in respect of the revised history of the patient. His ideas were very much in keeping with the team looking after the patient on initial presentation.

The patient was a 43-year-old woman. I would describe problem list first.

Problem list

#1 Skin rash

The lesions were circular, purplish, discrete, raised with an umbilicated central area. The lesions began as smaller discrete nodules that rapidly expanded. After several days, existing lesions developed a necrotic centre with circumferential erythema. The lesions eventually crusted over leaving large areas of eschar.

#2 Fever

#3 Tachycardia

#4 History of right breast cancer

#5 Acyclovir and ciprofloxacin administration

The main problem of this patient is fever and rash. Differential diagnosis is broad in fever and rash. However, I would think three main category, infection, neoplastic, and autoimmune. Characteristics of skin rash are likely infectious disease. Neoplastic or autoimmune is less likely. But neoplastic disease should be considered for background of this patient

Questions:

1) From the history and physical examination what would be your likely differential diagnosis?

Vascular: Less likely

Infection: Varicella, HIV, molluscum contagiosum, disseminated cryptococcosis, eosinophilic folliculitis, cutaneous anthrax

Neoplastic: (Recurrence of breast cancer)

Autoimmune: Sarcoidosis

Toxic: Less likely

Metabolic: Less likely

Trauma: Less likely

Degenerative: Less likely

Iatrogenic: Less likely

Idiopathic: Less likely

Congenital: Less likely

I would think varicella is the most likely based on the character of skin rash. The problem is this patient was a 43-year-old woman. Varicella is common in children. Moreover, this patient had history of breast cancer and acyclovir administration.

2) What are the two most important tests to confirm the diagnosis?

Tzanck smear for detecting multinucleated giant calls.

Direct immunofluorescent antibody (DFA) staining.

3) What is your chosen treatment?

Depend on following assessment, question 4.

4) What addition problem should you consider screening for in this patient?

Interstitial pneumonia as complication of adult varicella should be carefully monitored. Cancer screening including recurrence of breast cancer should be evaluated. Moreover, I would confirm pregnancy test.

The Answer

The team caring for this patient were very concerned about an infectious disease such as varicella and even cutaneous anthrax, despite no history of there being any exposure to the latter infectious disease. Therfore, she was nursed with full barrier protection as a precautionary measure.

Her laboratory studies were normal except for a neutrophilia. Varicella IgG was present and IgM was absent suggesting previous infection. Autoimmune serology including ANCA was negative.

Blood cultures were negative.

The patient had the lesions tested for varicella zoster with viral cultures, which were negative.

Chest radiograph was normal.

CRP was 13.6 and ESR was 17mm/hr.

She developed secondary staphylococcal infection as evidenced by impetigo and positive skin cultures. She was commenced on ceftriaxone.

She was reviewed by the hospital infectious disease specialist and dermatologist respectively, who both considered infectious, autoimmune and primary dermatologic disease.

The dermatologist also considered Acute Febrile Neutrophilic Dermatosis (Sweet's Syndrome) in view of the presentation, background history, fever and neutrophilia.

The patient therefore underwent a skin biopsy which confirmed the histopathology consistent with Sweet's Syndrome. She also met the proposed criteria for Sweet's Syndrome (see below).

She was commenced on corticosteroids orally (Prednisolone 60mg per day) with resolution of her symptoms and the lesions over several days. She was discharged home with outpatient follow up.

In view of her history of metastatic breast cancer, a search for secondary causes of Sweet's Syndrome such as a recurrent malignancy, would have been considered appropriate.

Sweet's Syndrome

Described by Robert Sweet 1964: A reactive process characterised by the abrupt onset of tender red-to-purple circinate plaques.

Usually occur on the

• extremities
• head
• neck

and typically are accompanied by fever and peripheral neutrophilia.

Pathophysiology

Neutrophil mediated hypersensitivity reaction to systemic factors, which may include, haematologic disease, infection, or drug exposure.

Evidence suggests that Sweet’s Syndrome is a cytokine T-cell-mediated disease with secondary and only temporary activation and participation of neutrophils.

Primarily skin affected but lung and kidney can be involved.

Frequency

Uncommon condition; several hundred reported cases in literature ~2.7 cases/million (Scotland) Kemmett et al 1990

~10-15% cases in setting of malignancy (which includes recurrent breast cancer) but most cases are idiopathic and benign.

Females predominantly affected (F:M 2-3:1) esp. non-malignancy associated Sweet syndrome.

Age at onset

• Females 30-50
• Males 60-90

Causes

• Idiopathic (~70% cases)
• Haematologic Malignancy: CML, AML, MDS. Hodgkin disease, cutaneous T-cell lymphoma, NHL, multiple myeloma, and hairy cell leukemia.
• Non-Haematological Malignancy: Slight increase in genitourinary cancers, rectal cancer, oral / tonsilar cancer, breast cancer and osteosarcoma.
• Infection: Streptococcal pneumonia, Yersinia infection. Atypical mycobacteria.

Drugs

G-CSF- well established cause

Possibly
Septrin
all-trans retinoic acid
minocycline

Anecdotal - Limited reports of drug associations include
lithium
furosemide
hydralazine
carbamazepine
levonorgestrel/ethinyl estradiol.

Systemic Disorders

15% cases of Sweet’s Syndrome

Most common association
Crohn’s Disease
Ulcerative Colitis

Sjogren’s, Behcet’s, RA, SLE , undifferentiated connective tissue disease all associated with Sweet’s.

Proposed diagnostic criteria include the following:

Both major criteria must be met in addition to two of the four minor criteria.

Major criteria

1 Acute onset of typical skin lesions
2 Histopathological findings consistent with Sweet’s syndrome

Minor criteria

1 Fever > 38°C or general malaise
2 Association with malignancy, inflammatory disorder or pregnancy or antecedent respiratory or gastrointestinal infection
3 Excellent response to systemic corticosteroids or potassium iodide (KI)
4 Abnormal laboratory values at presentation (three of four required: ESR > 20 mm; leukocytes > 8000; neutrophils > 70%; positive C-reactive protein)

(Rook's Textbook of Dermatology, Seventh Edition)

Treatment

Steroids!! Usually Prednisolone 1.0mg/kg/day -> Lesions should resolve <14>

Other treatment modalities

• Colchicine 1.5 mg/day
• Dapsone 100-200 mg/day
• Clofazimine 200 mg/day
• Cyclosporin A 5-10 mg/kg/ body weight/day
• Indomethacin 50-100 mg/day
• Naproxen 750 mg/day
• Doxycycline 200 mg/day

von den Driesch P. 1994

Prognosis

• Outcome depends on the underlying condition
• Recurrence may occur in up to 50% of patients
• Most likely in cases associated with haematological malignancy or drug reaction.

Take Home Message

When you see a patient with an unusual condition such as this, please involve the dermatologist as soon as possible for advice on the likely cause and for a skin biopsy to be taken.

Without a biopsy, despite the best problem list and differential diagnosis it can be difficult to establish the diagnosis even for the best of diagnosticians.

Certainly the history of the acute onset, location and progression of the disorder help to point to Sweet's syndrome as a possible diagnosis but a skin rash with fever has a wide differential. Hence, a biopsy is the very best way to establish the cause -- tissue is the issue!

Much of dermatology is pattern recongition and it can be difficult even for most senior doctors.

I would like to thank Prof Matsumura for his excellent attempt at diagnosis in this rare case. His suggestions were very good and would have led to the diagnosis through a skin biopsy as inferred from the two tests proposed. Moreover, checking for recurrent cancer and pregnancy showed good lateral thinking and were correct. Well done.

A Case For June 2009: Back with a difficult case!

Dear Bloggers

I am so sorry I have not been keeping up the blog. Life has been somewhat busy ! However, I have a great case for you. Have a go at trying to answer it. Answers in the near future.

A 43 year old Caucasian hospital secretary presented to a hospital with the following:

• Skin rash
• Fever

The lady was usually in good health when she developed an acute rash that commenced on her neck, and progressed to her face, trunk and upper + lower extremities over several days.

The rash was not painful or itchy. She described the rash a 'spotty', 'red' and 'knobbly'.

She went to see her local doctor who thought she might have an infection and prescribed her oral aciclovir and ciprofloxacin. However, rather than the rash regressing, it progressed rapidly at the dismay of the patient. Two days after receiving the antimicrobial therapy the patient developed a low grade fever of 37.6 degrees. The patient attended her local doctor again who referred her to the internal medicine team of the general hospital.

Her only previous history had been a mastectomy for carcinoma of the right breast in 1995 with dissection of 1 lymph node. She had been treated post-operatively with radiotherapy and chemotherapy (chemoradiation). She had been deemed disease free at her last outpatient follow-up.

She had one child aged 10 years old born via a normal vaginal delivery. Her periods were regular every 28 days with 5 days bleeding. Her last menstrual period had been one week before (which had been normal) and she denied pregnancy. She used barrier contraceptive with her husband. She and her husband were monogamous.

She had otherwise been well with no recent infection. She had not traveled recently, there were no pets at home and no recent contact with animals. She had no contact with patients in the hospital where she was employed. Other members of her family were unaffected. She had no unusual hobbies.

She denied taking any medications, herbal supplements or over-the-counter (OTC) drugs prior to the onset of her symptoms. Her daily food intake had not changed. She denied using any new jewellery or washing powders.

She had no relevant family history. She was a non-smoker and drank alcohol only occasionally.

On review of systems, she denied any cardiovascular, respiratory, abdominal, musculoskeletal, urogenital, CNS-PNS or endocrine symptoms. She particularly denied weight loss, appetite change or night sweats.


On Examination


VITAL SIGNS: BP 120/80mmHg, Pulse 108 / min & regular, Respiratory Rate 14/min, T 37.4 degrees C, SpO2 98% breathing ambient room air.

GENERAL: Looked well but slightly shaky. No JACCOL

HEENT - Nil focal except for rash (see below). No goitre.

CVS - Pulse volume and quality: normal, JVP not elevated, no carotid bruits, No heaves or thrills, S1 + S2 present, No S3 or S4, gallop or pericardial rub. Peripheral pulses present throughout. No evidence of DVT in the lower limbs.

RESP: No tracheal tug or deviation. Normal chest expansion. Percussion resonant. Normal vesicular breath sounds.

ABDOMINAL: Soft, non-tender, no masses or organomegaly. No hernial orifices and no groin lymphadenopathy. Rectal exam was not performed.

BREAST EXAM: Left breast normal - no masses, no skin abnormality, no abnormal nipple discharge and no axillary lymphadenopathy. Right mastectomy scar present. No evidence of recurrence. No axillary lymphadenopathy.

SKIN: The following pictures show the rash. The lesions were circular, purplish, discrete, raised with an umbilicated central area. The maximum diameter was about 1cm. The lesions began as smaller discrete nodules that rapidly expanded -- please see the yellowish smaller nodules in the lower part of the picture (below)


After several days, existing lesions developed a necrotic centre with circumferential erythema. The lesions eventually crusted over leaving large areas of eschar from involuting coalesced lesions over the shoulders and proximal lower limbs. Fresh lesions continued to develop.


Questions:

1) From the history and physical examination what would be your likely differential diagnosis?

2) What are the two most important tests to confirm the diagnosis?

3) What is your chosen treatment?

4) What addition problem should you consider screening for in this patient?

Catastrophic Arthritis

The above photo was provided as an anonymous example of an all too common arthritic disease -- rheumatoid arthritis.

As can be seen the patient has boutoniere change in the left hand, ulnar deviation of the fingers from subluxation at the MCP joints.

There is also some telescopic changes of the fingers usually a feature of psoriatic arthritis. There were no psoriatic nail changes or skin abnormalities seen.

Elbows revealed RA nodules and dislocations. The shoulders were affected as were the knees, ankles and toes.

Despite these being 'classical signs' of RA, we should not be seeing this in this day and age. We should not be seeing this because there are very effective DMARDs available to suppress RA.

This patient, if newly diagnosed today would be started on methotrexate and the dose would very rapidly be titrated to the recommended dose of 15-25mg per week or maximum tolerated dose, with a starting dose of 7.5mg per week. Sometimes if oral MTX is not effective, subcutaneous administration is tried.

DMARD treatment should not be delayed. If the inflammatory changes can be suppressed within the first 6 months of symptoms onset (early RA) then the chronic debilitating features can potentially be avoided.

This patient was on combination treatment of methotrexate, bucillamine and prednisolone. However, the dose of MTX used in Japan is usually lower than that recommended in trials e.g. 4mg. Older 'add on' DMARD therapy such as bucillamine, the cousin of penicillamine, is also still used commonly.

With the advent of MTX, leflunamide and anti-TNF antibodies, the likes of penicillamine are now rarely used in the UK. However, occasionally, patients still use drugs such as anti-malarials (hydroxychloroquine) or sulfasalazine in the UK.

Patients should no longer get to a state of being disabled by an ultimately treatable condition.

There is a real need for more expertise in treating connective tissue diseases so that patients can be managed with the most effective drugs in line with current medical evidence.

The term 'burned out' RA which this patient might appear to have is a misnomer. RA is now considered to be a continuous disorder which does not burn out. Also, such patients have an increased risk of death compared to the rest of the healthy population. Hence, it is not merely an inconvenience, it increases morbidity and mortality.

The term of 'hit it hard and hit it fast' applieds to RA. If the therapy is delayed or insufficient to suppress the arthritis, patients can end up the very same as in the photo above.

Please read UpToDate 17.1 for the latest evidence on RA. Note that penicillamine is not recommended by UpToDate for modern treatment of RA.

Please consider.

-- Post From My iPhone

Translation of Pathology into Questions for History Taking

Dear Bloggers

I have often focused my blog articles on how to take a history. However, many junior residents come from medical school and are still uncertain how to ask the 'right' questions. It is not an easy thing being faced with a sick patient and then, miraculously knowing which questions to ask. However, in order to understand what questions we should ask in the very first place we need to fundamentally turn things upside down and think about the disease first and then work out what questions can stem from such diseases.

For example, a patient may present with chest pain. This should immediately make us consider the causes of chest pain that should never be missed, for example, acute coronary syndrome (ACS), aortic dissection, pulmonary embolism, pneumonia, pneumothorax, oesophageal rupture, to name but a few.

The direction of questions to the patient is totally dependent on the presenting complaint. Hence, when we consider ACS, we know that it causes crushing, severe chest pain with pain radiating to the neck, jaw, arms. There can be sweating, nausea, vomiting, collapse, palpitations etc. The duration of pain is usually defined as lasting more than 20 minutues.

Now, we need to translate such information into questions.

For example,
'Please tell me what the pain feels like' [open question]
'Does it feel like a heavy pressing feeling? Like an elephant sitting on your chest?' [closed question]
'Does the pain travel anywhere else?' [semi-open question]
'Does it travel to your neck, jaw or down your arm or arms?' [closed question]
'What time did the pain start? What were you doing at the time?' [open question]
'How long do you think you have had the pain?' [open question]
'On a scale of 1 to 10, 1 being almost no pain and 10 being the worst pain imaginable, where would you put this pain on that scale?' [visual analogue scale -- very important!]
'Have you had any other symptoms with this pain?' [open question]
'Have you had any nausea, vomiting, palpitations or loss of consciousness ?' [closed question]
'Have you had a pain the same as this before?' [open question]

The above example is a string of 'stock' questions for defining possible Acute Coronary Syndrome which then makes us consider the investigations and treatment even before the laying on of a stethoscope.

On the hand, the patient may say that the pain feels sharp when breathing, which takes us down the route of ALSO asking about causes of pleuritic chest pain. We still ALWAYS ask about the ACS, aortic dissection, oesophageal rupture questions as well. We DO NOT miss them out just because the pain sounds pleuritic. We go back to these other screening questions AFTER dealing with the specific questions for pleuritic chest pain.

Hence, 'Please tell me what the pain feels like' [open question] -- SHARP, WHEN I BREATH IN
'Do you have a cough or phelgm?' -- YES, I COUGHED UP SOME PHELGM
'What colour was the phelgm?' -- I AM NOT SURE.....
'Was it white, yellow, green, brown or red like blood?' -- ACTUALLY, IT WAS RED LIKE FRESH BLOOD
'Do you feel feverish or chilly?' -- NO
'Have you got any other symptoms?' -- YES, I FEEL A BIT BREATHLESS
'Can you tell me when it happened?' -- MMM, IT WAS SUDDEN, WHEN THE CHEST PAIN CAME ON
'Can you tell me how severe your breathlessness is? For example, are you breathless talking to me now or just when you walk?' -- I AM BREATHLESS WHEN I WALK
'Do you normally get breathless?' -- NO, I AM USUALLY OKAY TO WALK ANYWHERE WITHOUT A PROBLEM
'Do you feel any other symptoms?' -- SUCH AS?
'Well, do you have any palpitations of your heart? Does it feel irregular, fast or slow?' -- IT FEELS FAST AND IRREGULAR
'Have you noticed this problem in the past?' -- NO, I HAVE ALWAYS BEEN HEALTHY
'Have you been unwell recently?' -- NO
'Have you taken any recent long-haul flights?' -- YES, I FLEW TO AUSTRALIA FOR A SHORT HOLIDAY. THE FLIGHT TOOK 18 HOURS. I CAME BACK 3 DAYS AGO.
'Do you have any leg swelling? Any pain or redness of either leg?' -- YES, I NOTICED IT THIS MORNING. MY RIGHT LEG SEEMS SWOLLEN AND PAINFUL.
'Have you been diagnosed with any cancer recently? Or do you take any hormone replacements such as the contraceptive pill?' --NO
'Do any of your family have any history of blood clotting problems?' YES, MY MOTHER HAD A CLOT IN HER LEG IN THE PAST. SHE HAD TO TAKE WARFARIN FOR THE REST OF HER LIFE. THE DOCTORS DID NOT KNOW WHAT CAUSED IT IN HER DAY.

At this point, the diagnosis of deep vein thrombosis causing pulmonary embolism is pretty well established just from the history. The history also tells us that the patient has at least two risk factors -- remember Virchow's Triad? She has poor flow from a long-haul flight and a familial tendency to form clots [hence a change in blood viscosity]. Two out of 3 of Virchow's Triad predisposes to thrombosis. Again, from the history, it makes us consider the investigations and treatment even before laying on of the stethoscope.

After this history of the main problem, we still go on to ask about the other causes of pleuritic pain such as 'Do you have any history of tuberculosis?' 'Any recent history of a common cold e.g. running nose, earache, headache' -- remember Tb, typical pneumonia, viral infections etc, can cause pleural reactions and localised chest pain.

We also still ask about the diagnoses that should not be missed and hence, the previous ACS questions
'Does the pain feel like a heavy pressing feeling? Like an elephant sitting on your chest?' [closed question] -- NO
'Does the pain travel anywhere else?' [closed question] -- NO
'Does it travel to your neck, jaw or down your arm or arms?' [closed question] -- NO
'What time did the pain start? What were you doing at the time?' [open question] -- 8:30 THIS MORNING, I WAS WASHING THE DISHES.
'How long do you think you have had the pain?' [open question] -- AT LEAST 2 HOURS
'On a scale of 1 to 10, 1 being almost no pain and 10 being the worst pain imaginable, where would you put this pain on that scale?' [visual analogue scale -- very important!] -- 5/10
'Have you had any nausea, vomiting, palpitiations, loss of consciousness ?' [closed question] -- YES, PALPITATIONS ONLY BUT NONE OF THE OTHER SYMPTOMS
'Have you had a pain the same as this before?' [open question] -- NO, NEVER

Hence, the response of the above questions takes us away from ACS as the cause and keeps us pointing towards DVT-PE.

The specific questions for aortic dissection, oesophageal rupture and other pathologies still need to be asked so that they are not missed. It is best to be thorough. Sometimes, patients present with TWO pains, and both could be life threatening so it is only with the history being taken methodically that the cause of the different pains can be elucidated.

As can be appreciated, it is the presenting complaint that stems the follow-on stock questions in order to identify serious pathology so that a rapid diagnosis can be made and the correct treatment can be instituted.

From the above history, we are soon able to narrow down the diagnosis to DVT-PE by changing from open to closed specific questions. Once the critical diagnosis is considered, the physician seeks to establish the cause and risk factors for the problem. In doing so, when performing the physical examination, the physician would focus the examination on the cardiorespiratory system by looking for tachycardia, raised JVP, pleural effusions, crackles, signs of DVT in the lower limbs.

In view of the family history, the patient would be screened for familial coagulopathies, a D-Dimer would be checked and the patient would have an ECG to screen for ACS and ECG abnormalities associated with PE.
The patient would receive a chest radiograph to look for a widened mediatinum (screen for dissection), consolidation, effusions etc.
The patient would receive a spiral CT of the chest and a doppler ultrasound of the lower limbs and pelvis to look for thrombosis whilst receiving full treatment dose of heparin as soon as possible.

Hence, in summary, when we hear the chief complaint, we must immediately begin to think of diagnoses that fit the initial pattern. We must consider life threatening diagnoses first. When thinking of the pathology, consider how the disease can manifest. Then consider how those manifested problems can be explained by symptoms. Then pose those questions to the patient.

Explore all the serious pathologies before moving down the list on to the less severe and non-acute causes of the symptoms.

In the end, you will have taken a very detailed history and have many pertinent positive and negative symptoms and hopefully, a very focused history of the disease you have already considered at the very first mention of the chief symptoms. It is important though to take the history rapidly in the case of life threatening problems such as ACS. In such situations, it is often the case that the doctor takes the history whilst examining the patient :-o

At first it may be difficult to think in this way but with practice, being able to take a history will become easier in time. Remember though, read about your patients conditions and remember what they tell you. It will help you make diagnoses in your future patients too.

Please consider....

Physical Examination - Revisited ---- again

Dear Bloggers

I have been exceedingly busy recently ! However, I am back :-)

I wanted to reiterate the importance of the physical examination. One method of teaching from the UK involves taking no history from the patient and hence, using only observational skills to make a diagnosis! Although history can give the diagnosis in a high percentage of cases, the physical exam aids the physician to confirm or refute various differential diagnoses in certain circumstances e.g. the patient complains of palpitations but on the physical examination the patient has a normal pulse despite the patient still being symptomatic. On the other hand, the patient might complain of unilateral pleuritic pain, cough and sputum and the physical exam reveals a pneumonia. Hence, physical examination can be positively or negatively correlated to the history.

The purpose of performing the bedside exam without the history is to hone the skills of the residents to get them to look but also to recognise what they see. Observational skills are exceedingly important and are often under-utilised. For example, when starting the physical examination, perhaps the most important thing is to look around the bedside. Many items surround the typical patient e.g. portable toilet (maybe the patient is too weak or too breathless to walk), the walking stick, intravenous infusion (rehydration, antibiotics, other drugs), oxygen via mask or nasal specs, the patient's regular drugs! These elements give the physician an idea of the patient's general status and functional capacity. They can also reveal the patient's previous medical history and tell you what is wrong with them! For example, a recent patient had a mitral valve murmur and had an infusion of gentamicin running into a peripheral vein. The immediate diagnosis to consider was infectious endocarditis!

Looking for the urine bag can provide information about the patient's vascular state and type of illness- is there urine? Check the colour -- e.g. blood, coke coloured (glomerulonephritis), orange (liver disease / Tb drugs), purple (UTI), green (propofol, UTI). Concentrated urine of small volume suggests hypovolaemia before even touching the patient.

Looking at the patient at the end of the bed generally can give clues -- general state e.g looks well / unwell, weight loss (backs of the hands, temporal regions, upper arms and legs), colour of the skin / sclerae at a distance e.g. jaundice. Many clues about the patient can be picked up like this to make a preliminary opinion of the patient's condition before even laying a hand on the patient.

The UK way of examination, after general inspection, starts with the hands. The hands are an important part of the physical exam -- the type of handshake might indicate a neuropathy or myopathy. Unilateral wasting of the dorsal interossei might suggest a unilateral Pancoast tumour of the lung. Checking the fingers for clubbing can very quickly narrow the problem down to specific cardiac, respiratory or abdominal causes. Many other signs are present in the nails which are beyond this talk today. However, having a combination of signs may overlap with just a single condition and give the diagnosis or there may be separate diagnoses! For example, a recent patient with clubbed fingers also had Terry's nails, which when both present suggests liver disease. The patient had mild scleral jaundice and was unkempt. The resident rightly considered alcoholic liver disease, and he was correct. The liver was markedly enlarged and firm.

Checking the nail folds is imperative because infarcts may be seen in addition to capillary loops (seen with an opthalmoscope) which might indicate several forms of vasculitis or other rheumatological conditions. Of course, checking the digits may provide the diagnosis of rheumatoid arthritis or osteoarthritis. Asking the patient to extend the hands at the wrists with spreading the fingers can help identify those patients with encephalopathy e.g. liver failure, uraemia, CO2 retention.

Checking the pulse is not just counting the rate per minute. Feeling the volume is important. It may indicate the slow rise of aortic stenosis or the fast upstroke and immediate loss of the Waterhammer pulse of aortic regurgitation. A low volume 'thready' pulse may indicate poor cardiac output or hypovolaemia. The jerky pulse may even suggest HOCM at the wrist!

Checking the skin turgor can help indicate the fluid status of a patient although it is not so accurate in the elderly patient. However, a combination of signs e.g. thready pulse, tachycardia, cold digits, small volume concentrated urine in the catheter bag in addition to poor skin turgor indicate hypovolaemia. You don't need the BUN and Creatinine to tell you that. information as physical examination does just fine. The use of lab data in such a circumstance is to know the extent of the derangement :-)

Moving up to the head, the sclerae can be checked -- they might show anemia, jaundice, haemorrhages etc.. Again the mouth and throat can provide information. Checking the mucosal surfaces may reveal the Kaposi sarcoma or the lateral border of the tongue may have the Oral Hairy Leukoplakia of AIDS. The presence of white exudates on the mucosa and tongue suggest candida and then one must consider the DDx of why the patient has got it e.g. immune suppression from steroids, DM, AIDS. Has the patient been using recent antibiotics. Mucosal bleeding may be present indicating possible thrombocytopaenia!

Telangiectasia on the tongue, under the tongue and on the face with the presence of spoon nails 'koilonychia' should lead one to consider the rare diagnosis of Osler-Weber-Rendu (Hereditary Haemorrhagic Telangiectasia) with iron deficiency anaemia.

The facial skin can give a wealth of information. One might see the purply-red cheeks of SLE! However, remember that in an elderly patient with swollen legs, purple lips and purple fingers with the facial 'flush' is more likely to be due to low cardiac output e.g. CHF, rather than SLE!

Checking the neck can provide further information - the JVP being elevated and evaluating the wave form e.g. a wave or v wave, can tell use which problem may exist e.g. tricuspid regurgitation. Observing the neck for the carotid pulsation may reveal Corrigan Sign (common) and DeMusset's sign (head nodding with each pulsation -- rare). If you do see this sign or suspect aortic regurgitation then go back and look at the hands again. Try and find Quinke's Sign. I have found Quinke's sign in many patients simply because of the suspicion of AR through these ancillary signs and a suggestive murmur. Unless you look you will not find.

Checking the earlobes can reveal Frank Sign -- the diagonal earlobe crease suggestive of coronary artery disease although this depends on the population in question. The highest association is in caucasian patients.

The chest surface examination can reveal spider naevae and gynaecomastia of chronic liver disease, excoriations due to pruritis or tattoos and old scars amongst others. Looking at the skin teaches us about the patient's present and past.

Abdominal inspection may show obvious distension, eversion of the umbilicus, and caput Medussa of chronic liver disease.

The lower limbs can reveal similar features from the hands e.g. Clubbing, Terry's nails. However, specific rashes may occur which can give a clue about the illness e.g. petechial haemorrhage may suggest low platelets or a vasculitis. The presence of palpable, painful, multifocal erythematous lesions may suggest erythema nodosum with its respective differential diagnosis.

Notice, no chest or abdominal organ has been palpated, percussed and no stethoscope has been placed on the patient in the above examples of examination. All of the above signs can be found on inspection and point towards various diseases. Of course, examination of the heart, lungs and abdomen should be performed on a normal basis as well. However, what I am trying to emphasize is that physical examination is not just focusing primarily on the major organs. It is also looking at all the other areas of the body, which are often under appreciated, to try and pick up relevant clues which may relate to the problem of the major organ and thereby provide the clinical diagnosis at the bedside based on pattern recognition of disease.

Observational physical examination skills training, with a senior doctor who can then point out the relevant signs if the resident misses them, leads to improvement in recognition skills by the residents. By explaining the history to the resident after their finishing the examination, reinforces the physical signs teaching. Not only that, it is really exciting to see as things unravel.

For those medical educators out there, you may wish to consider doing this training with your residents. It can be illuminating to hear the correct diagnosis come forth without a word of history being heard and not a lab test or scanner in sight :-) Please consider....

An old disease in modern times -- be safe, not sorry.

Dear Bloggers

It is occasionally the case that a patient is admitted to hospital with because of an abnormal chest Xray showing upper lobe infiltration. History and physical examination are of prime importance because they can identify the possible causes and associated risk factors related to the abnormality.

Without taking a detailed history, you may be missing a serious diagnosis. For example, as a case vignette, an elderly lady was admitted to a hospital with worsening dyspnoea. She had a background of end-stage COPD from 80 pack-years (Brinkman 1600) of smoking.

Unfortunately, the history was incomplete (and therefore so was the subsequent assessment and plan) because the resident had failed to elicit from the patient that she had an active cough and sputum.

The chest radiograph revealed bilateral upper lobe infiltrates, a simple pneumothorax and hyperinflation consistent with COPD.

The patient was admitted for 'observation' to an open ward with other patients and was not wearing a face mask.

Examination revealed an emaciated patient with a hyper-expanded chest. She was mildly febrile (37.5 deg C), respiratory rate 24/min, HR 90 regular, BP 130/80mmHg and O2 Sats 98% on 2L oxygen via nasal cannulae. Lymph nodes were not palpable. There was increased percussion sound throughout the chest but reduced air entry in all lung fields and crackles at the left apex.
The rest of the examination was within normal limits.

In view of the high prevalence of tuberculosis in Japan, this should be the very first consideration in any patient with upper lobe infiltrations with pneumothorax. Although COPD is the commonest cause of pneumonthorax (70%), the concommittant existence of both radiographic features point primarily towards Tb. At the bedside, more history was taken and it was revealed that the patient did indeed have a cough and sputum. In fact, she coughed up sputum right in front of the medical team.

There are several other causes of upper lobe infiltrates defined by the following mneumonic:

S - Sarcoidosis, Sulfa drugs, Silicosis
H - Histoplasmosis
I - Idiopathic
R - Radiation induced
T - Tuberculosis (post-primary)

C - Chronic allergic alveolitis
A - Ankylosing spondylitis, Aspiration penumonia
P - PJP (when using pentamidine nebulisation), Progressive Massive Fibrosis
E - Eosinophilic granuloma

On closer inspection of the chest radiograph, the patient had vertebral body changes with calcified ligaments that might be consistent with ankylosing spondylitis. However, sometimes, severe facet joint osteoarthritis can present in this manner in the elderly as can Diffuse Idiopathic Skeletal Hyperostosis. Ankylosing spondylitis usually presents in a younger age group and is relatively rare. Osteoarthritis is very common and a more likely explanation for the 'bamboo spine' changes.

However, given the above scenario, what is the likely cause for bilateral upper lobe infiltration in a patient with COPD?

Of course, atypical presentation of a community acquired pneumonia is possible. e.g. Streptoccous pneumoniae. Moreover, Klebsiella pneumonia, H. influenza, Pseudomonas or even post-influenzal staphylococcal infection can present in such a way. Atypical pneumonia should also be considered. Of course, this patient might have aspiration but bilateral infiltration with the absence of lower lobe infiltration would make this diagnosis somewhat tenuous.

However, the above infections can be diagnosed rapidly and treated quickly and effectively with standard antimicrobial agents. Tuberculosis on the otherhand is difficult to diagnose and requires multiple antibiotics for many months. Moreover, Tb is very infectious and has an infectivity rate of about 10% ! That translates to 1 in 10 persons becoming infected and developing active disease at some point during their life from a patient coughing up active Tb into a space where the Tubercle bacilli remain airborne.

Hence, anyone with even the remotest suspicion of active tuberculosis who is coughing up sputum must not be placed on an open ward. They must be admitted directly to an isolation room with negative pressure (air is sucked into the room). Full protective garments should be worn by the medical staff including the 3M filtration face masks.

Such patients should be kept isolated until such time that tuberculosis has been excluded. Please see any good infectious disease book for the work-up of tuberculosis e.g. Dr Makoto Aoki's Infectious disease book.

It is no good trying to make an simple diagnosis e.g. aspiration pneumonia, without first excluding the serious/life threatening diagnoses that one 'should not miss'.

As I have heard many times in Japan 'In any patient with a fever, always consider tuberculosis'. I think that is a very apt saying and which I fully support.

Further widely quoted advice is 'rule out Tb before starting the steroids'. Again this is very important. Corticosteroids can reactivate latent Tb or worsen existing Tb. So be careful to check the PPD skin test, sputum examination and culture before pulsing your suspected interstitial pneumonia patient with methylprednisolone which might actually be Tb.

Usually, interstitial pneumonia patients can afford to wait for several days before starting the steroids giving enough time for the preliminary Tb examinations to be done. However, if steroid therapy is necessary because of worsening disease or for example, the patient has an 'infective exacerbation of COPD' requiring steroids with a suspicious CXR suggesting Tb, anti-Tb therapy should be commenced with the steroids (preferably after Tb samples have been taken) in order to treat this suspected infection along with that of the the acute illness. If Tb is later ruled out by tests, the Tb therapy can be stopped. It is better to be safe than sorry.

This is supported by UpToDate 17.1 in the section under Major Side Effects of Systemic Glucocorticoids which says 'Conventional wisdom suggests that any patient with a positive PPD skin test, a suggestive chest radiograph, or a strong family history of tuberculosis should receive antituberculosis prophylaxis prior to, or concomitantly with, glucocorticoid therapy'.

You cannot take the risk of having a single patient on an open ward with active Tb. Yes, it may cause the nursing staff / doctors / managers some extra work in order to organise an isolation room, but by not doing so puts many people at risk of Tb exposure.

Please consider....