Nasty Pneumococcus

This case has been anonymised to protect patient confidentiality.

A 60 year office worker presented to his local clinic with a fever and symptoms of a common cold.

He was provided with some antibiotic treatment but over the next few days, his status declined further with headache and pain in the back of his neck. He also developed some intermittent hearing loss that progressed to absolute deafness on the day of his admission.

On admission he was unable to hear but was able to express his pain.

Examination on admission revealed a temperature of 36.4 degrees, pulse 90, BP 128/70, respiratory rate of 20/min, SpO2 of 96% on 6L oxygen

CV examination was normal.

Resp examination showed reduced excursion of the chest on the Left side, dullness and reduced breath sounds. Crackles were audible only at the Left base.

Abdominal examinatiom was reported as normal except for a slightly palpable liver edge which was apparently tender.

CNS examination was reported as all normal including No Neck Stiffness and Negative Kernigs signs.

However, he had complete deafness albeit that Weber's and Rinne's tests had not been attempted to determine if it was conductive or sensorineural deafness, although with such a rapid history and bilateral hearing loss, it is likely to have been sensorineural hearing loss.

Bloods revealed WCC 12, Differential low neutrophils and low Lymphocytes. CRP was over 30. BUN 16 creat 0.76. Liver function showed slightly raised bilirubin of 1.9, AST 90, ALT 80, Alb 26. INR 1.3. FDP / D-Dimer had not been done.

Lumbar Puncture showed an opening pressure of 50cm H2O, WCC of 9, 8 were Lymphocytes and 1 was a PMN. Protein was over 150 and Glucose of ZERO. Diplococci were seen on gram stain.

Blood cultures grew Streptococcus pneumoniae.

CXR revealed a severe left upper lobe pneumonia with there being some smaller right sided perihilar consolidation as well.

CT head showed dilated lateral ventricles but no cerebral matter effacement.

When reviewed, the patient's family were able to provide a wealth of information to fill in the history, which I have included above. He had recently visited an onsen but he had had no foreign travel. He had been a smoker of 3-4 cigarettes per day, but he had stopped 6 months previously.

On examination, the patient appeared severely unwell and he appeared in pain.

His eyes were screwed up and he was cold and sweaty despite being on a warm ward.

CV and Resp exams were as above BUT Respiratory Rate was increased to 30.

Abdominal exam revealed a large, tense bladder which was stony dull to percussion and a dull liver edge on percussion. Traub's Space was also dull suggestive of splenic enlargement although no spleen was palpable.

CNS examination revealed spontaneous eye opening, localisation to pain but no speech (GCS= 10/15). Pupils were consticted to approx 3mm equally but fundoscopy was not possible due to the pupils being small, continuous eye motion, intermittent eye closure of the patient and cataracts.

The patient clearly had neck stiffness as he winced on having his neck turned and a similar situation occurred on testing Kernigs making it Positive.

Reflexes were increased in the upper limbs but completely absent in the lower limbs although the patient appeared to have power to withdraw in both upper and lower limbs. Plantar reflexes: left foot normal, right foot equivocal. Other ways to elicit the plantar reflex such as achilles tendon pinching and flicking the medial malleous were Negative.

Skin revealed no rash.

Clinical Impression:

Having considered the clinical case and physical findings with lab data the following diagnoses were considered:

1) Pneumococcal Pneumonia

2) Pneumococcal Meningitis with Secondary Communicating Hydrocephalus due to probable Arachnoid Villi blockage in the Superior Sagittal Sinus from the infection. The possibility also exists of superior sagittal sinus thrombosis.

3) Bilateral nerve deafness due to pneumococcal meinigitis and hydrocephalus.

4) Liver dysfunction from sepsis / DIC / ? underlying liver disease

5) Pneumococcal Septicaemia and possible DIC

6) Urinary Outflow Obstruction possibly due to severe illness / autonomic dysfunction / Reduced level of Higher Function due to meningitis and hydrocephalus

Suggestions

It was suggested that the antibiotic therapy be continued with Ceftriaxone 4g/day and Vancomycin, although it was not entirely convincing that intravenous Erythromycin that was also commenced would be effective especially as this antibiotic is Bacterostatic and Not directly Bacterocidal.

The patient was also given Dexamethasone which again is the correct treatment in such circumstances.

It was advised on passing a Foley urinary catheter and measuring hourly urinary output especially as he had a systemic illness.

The patient clearly had developed a System Inflammatory Response Syndrome (SIRS).

It was also advised that the neurosurgical team should be contacted for advice as the patient might require a ventriculoperitoneal shunt if the raised pressure continued to be a problem.

In view of the raised INR and abnormal liver tests and with DIC having not been excluded it would not have been safe to consider heparin for possible superior sagittal sinus thrombosis and this would have need an MRI scan first.

I suppose the lessons to be learnt here are:

1) Get as much history as you can from family if the patient can't communicate

2) Don't rely on observations taken on admission as they can change and deteriorate; DO YOUR OWN OBSERVATIONS TOO WHEN YOU REVIEW THE PATIENT.

3) Look at your patient's eyes to see if they are in pain when examining as in this case the neck stiffness and Kernig’s that were 'negative' were in fact Positive.

4) Always consider catheterising the severely sick patient as it is essential to relieve bladder pressure and monitor urine output as it is a very sensitive way to determine deterioration in renal function

5) Always consider putting Meningitis patients on an HDU/ICU for intensive nursing care

6) Always think of using Steroids in such cases; the evidence these days suggests using steroids.

7) Remember that patients can develop DIC, so obtaining FDPs, D-Dimer and a Blood Smear looking for MicroAngiopathic Haemolytic Anaemia (MAHA) may provide useful clues.

Update: The organism was later found to be a Penicillin Sensitive Streptococcus pneumoniae.

It was then suggested to stop the Vancomycin in view of the organism being a PSSP and also worsening renal function. It was also suggested to switch from ceftriaxone to Benzylpenicillin- the best therapy in such instances.

Moreover, the patient's conscious level decreased perhaps in part due to hypernatraemia that developed but also from a possible superior sagittal sinus thrombosis. MRI and MRV were suggested imaging to be obtained.

DIC was excluded in the end, and in fact, the liver function initially worsened before beginning to improve.

The patient did eventually make an adequate recovery but required a VP shunt due to worsening pressure and underwent physiotherapy.

Answers to Quiz: Ulcerative Colitis

As promised, I have provided below the answers to the Quiz that I set for you last week.

I have had a few responses with basically the right answers, so very good.

However, I will list in detail what I consider to be the important points.

Question 1:

What is the eye sign? EPISCLERITIS.

A very uncommon manifestation of Ulcerative Colitis although it may also be seen in other systemic inflammatory conditions e.g. RA, SLE, PAN, Wegeners, Relapsing Polychondritis, sarcoidosis.

Infections can also cause episcleritis and include opthalmic zoster, HSV, Lyme disease, syphilis, TB.

Question 2:

What is the lower extremity skin signs and what are the possible causes of it? ERYTHEMA NODOSUM.
This sign usually occurs on the lower limbs and is typically painful to touch. In this patient, his presented without pain which is somewhat strange. Unfortunately, no biopsy of the skin changes was performed and hence, this is only my clinical opinion.

Other causes of E.N. include:

DRUGS: Sulphonamides, Contraceptive pill, Penicillin, Salicylates

INFECTION: Atypical pneumonia e.g. Mycoplasma, Strep infections, Rheumatic fever, TB, Leprosy, Yersinia Enterocolitica, Bartonella infx, Syphilis, Toxoplasmosis, Coccidioidomycosis

INFLAMMATORY: Sarcoidosis, Ulcerative Colitis, Crohns Disease, Behcets disease

MALIGNANCY:Lymphoma, Leukaemia

PHYSIOLOGIC: Pregnancy

Question 3:

With the history and examination in mind, what is the likely diagnosis or at least, provide some differential diagnoses?

A two month history of bloody diarrhoea of frequency of up to 10 x per day one must consider inflammatory bowel disease although bowel infection, vasculitis and even malignancy should be considered.

With a new onset of fever, episcleritis and erythema nodosum there are few conditions that could cause all of these manifestations.

I consider that Ulcerative Colitis is the top dignosis here although Crohns disease is another consideration. It is unlikely to be Behcets as the patient had no genital ulceration and no mouth ulceration. However, it is good to consider this diagnosis as it is considered to be more common in Japanese than caucasians.

Question 4:

What investigations should be done e.g. radiological / microbiological, etc...? ABDOMINAL XRAY, COLONOSCOPY WITH BIOPSY, STOOL CULTURE AND WHITE CELL EXAMINATION.
Patients with flares of UC should have an abodominal Xray if they have a distended abdomen to exclude a Toxic Megacolon which can occur in up to 10% of Severe Flare Ups as in this case. A Colonoscopy would provide a direct examination of the bowel mucosa allowing for histological samples to be taken for diagnosis. Stool culture MUST be done to exclude Clostridium difficile infection and other causes of bloody diarrhoea (Salmonella, Shigella, E.coli, Yersinia, Campylobacter etc..) as infection can cause exacerbations of UC. White cell examination can be useful but all this will do is prove that there is either inflammation or infection.

Question 5:

What treatments should be commenced on admission for this patient? STEROIDS and METRONIDAZOLE (FLAGYL). This patient had already been given a diagnosis of UC and had been taking Mesalamine and Sulphasalazine and no treatment alterations had been instigated on admission. It was clear to me that this was a severe flare of UC (>6 bloody stools per day, extra-intestinal manifestations and fever) and that steroids were needed. Moreover, it was not clear whether the patient also had a superimposed GI infection. Hence, my suggestions were of Oral Prednisolone plus Rectal Steroids in addition to Oral Metronidazole.


For those physicians that got the right answers-- Well Done.

There is an excellent review on the investigation and treatment of UC in the British Medical Journal and please have a read!! BMJ Vol 333. 12 Aug 2006. Pages 340-343.

JVP and the ECG

I have been unable to update my blog these last few days as I have been trying to get the new Microsoft Windows Vista to work properly. Having finally succeeded I have been able to update my blog today.

I want to mention something about the Jugular Venous Pulse (JVP) or Distension as the termed is coined elsewhere.

This physical sign is often missed or not even appreciated and through my daily teaching, the junior doctors are now looking for the JVP, and in some cases, it has proven a great diagnostic sign especially with the added help of an ECG (shin-densu).

The JVP is an estimate of the pressure of the venous circulation. It can be raised by many processes but particularly heart failure and atrial fibrillation.

The JVP should only be read with the patient at an incline of 45 degrees and not flat. Hence, you need to sit your patients up, and if they have severe cardiac or respiratory disease, they should be sat up already!

The JVP is measured vertically from the manubriosternal joint (sternal angle) to the top of the JVP wave in centimetres with the head turned to the left and with the physician examining from the traditional right side of the patient. A normal JVP <4cm.

A JVP should be seen as the superficial vein becomes distended over the sternocleidomastoid muscle area. It has a double pulse for every arterial (carotid) pulse. On sitting the patient vertically, unless the problem is very severe, the JVP should disappear. Also, on pressing the liver, the JVP should be seen to rise (Hepatojugular reflex-- I almost never do this as it can be painful and restrict breathing). I also occlude the jugular vein from below upwards thereby allowing me to differentiate whether the raised pressure is truly from the heart or whether it is simply due to filling from the cranial venous circulation.

The JVP has two waves, the first due to blood regurgitating during atrial contraction as it empties into the ventricle and the second as the atrium refills with blood before the ventricle relaxes and the tricuspid valve still remains closed. These are termed as 'a' and 'v' waves respectively.

Hence, the JVP can be predominantly raised with the 'a' wave or the 'v' wave but for the beginner, just seeing if the JVP is generally raised is the important thing.

JVP should be assessed in all patients and it should give a diagnostic clue in conditions such as CHF, large pulmonary embolism, atrial fibrillation, valvular disease, COPD and other chronic respiratory diseases.

A clue as to the cause of the raised JVP can be sometimes seen on the ECG.

For example, today I saw an elderly lady with COPD. Before seeing her I reviewed her ECG which showed peak / tall 'p' waves consistent with the term p pulmonale and hence, right atrial enlargement. Her arterial blood gas revealed a respiratory alkalosis and profound hypoxaemia of 55mmHg. Examination of her JVP revealed large venous waves (the rapid upstroke and rapid down stroke of the venous blood consistent with Tricuspid Regurgitation). She had no obvious right ventricular heave and no murmur as it is likely she has complete TR. She had no peripheral oedema.

The history of smoking, the profound hypoxaemia, ECG changes of the 'p' wave led me to conclude that she had developed Type 1 Respiratory Failure and chronic pulmonary vascular vasoconstriction had caused RA enlargement and TR. This would be consistent with Cor Pulmonale.

Sometimes the ECG will show RV strain (ST depression and T wave inversion) in the RV leads e.g. V1, V2, V3, aVR and with the presence of p pulmonale, hypoxaemia one should also consider pulmonary embolism although other diagnoses such as pulmonic stenosis, mitral stenosis, primary pulmonary hypertension, cardiomyopathy should also be considered amongst others.

Finally, examples of predominant 'a' wave elevations in the JVP include: pulmonary hypertension, pulmonary stenosis.

Large 'a' (Cannon) waves are seen in complete heart block, atrial flutter, single ventricle pacing, ventricular arrhythmias/ectopics.

Absent 'a' waves in atrial fibrillation (no proper atrial contractions!)

Large systolic 'v' waves are seen in Tricuspid Regurgitation.

JVP can be raised for other reasons such as fluid overload, cardiac tamponade, SVC obstruction, constrictive pericarditis.

Good hunting for the JVP!!!

History and Physical Quiz: I need your Answers!!!!

Today I am going to do something different. I am setting you all a quiz!

I will give you a short history and show you the physical signs that I picked up on this patient and please send me your answers to the questions I have posed at the end of this blog.

History

This is a 41 year old male computer worker who developed bloody diarrhoea of up to 10 times per day. The diarrhoea was non-painful and he experienced no abdominal pain. He had these symptoms for 2 months prior to coming to the hospital.

He had recently developed a fever prior to admission and in fact, that was the reason for him seeking medical intervention on this occasion. He denied any shivers or shakes. He noticed the skin on his legs had become discoloured but they were not painful.

He had no chest pain, dyspnoea, cough, sputum or haemoptysis. No genitourinary, joint, throat, or cranial symptoms.

He denied eating raw or poorly cooked foods and he denied any foreign travel. He had no pets at home. He had a similar episode of this in the recent past and was taking some medication but he could not remember the name of his diagnosis or treatment when he was admitted to hospital.

He had no recent weight loss, night sweats or loss of appetite. He was taking no anti-coagulant drugs or Non-Steroidal Anti-Inflammatory Drugs. He denied any previous peptic ulcer disease and he drank no alcohol. He had experienced no haematemesis and had no symptoms of gostroesophageal reflux disease (GERD).

There was no family history of bowel disease or cancer.

On examination: He looked relatively well. BP and Pulse were stable. Temp 38.0 degrees C. Resp Rate 14/min and O2 sat 98% on room air.

No Jaundice, Anaemia, Clubbing, Cyanosis, Oedema, Lymphadeopathy (No JACCOL)

CVS: pulse 80/min, regular. BP 120/80 mmHg. JVP was not raised. Heart sounds 1 + 2. No added sounds or murmurs. No evidence of DVT in the lower extremities.

RESP: Trachea central. No tracheal tug. Expansion normal bilaterally. Percussion resonant throughout and Auscaultation revealed Vesicular breath sounds.

ABDO: Soft, non-distended, non-tender, no organomegally. Bowel sounds normal. No signs of chronic liver disease. Rectal examination: fresh red blood, no obvious discharging fistula orifices.

JOINTS: Normal range of movement. Non-tender and no swelling.

EYES: See Photograph

SKIN: See Photograph

NO BLOOD RESULTS OR OTHER TESTS RESULTS ARE PROVIDED AS A DIAGNOSIS / DIFFERENTIAL DIAGNOSIS SHOULD BE MADE SOLEY ON THIS HISTORY AND EXAMINATION























































Question 1:

What is the eye sign?

Question 2:

What is the lower extremity skin signs and what are the possible causes of it?

Question 3:

With the history and examination in mind, what is the likely diagnosis or at least, provide some differential diagnoses?

Question 4:

What investigations should be done e.g. radiological / microbiological, etc...?

Question 5:

What treatments should be commenced on admission for this patient?

I will publish all answers and I will provide you the answers in one week from today!!

Good Luck!!!

Nails-- The Looking Glass Into The Body

Splinter Haemorrhages

Good day to you all and I must say what glorious sunny weather we are now having this month-- only February and I have already seen trees producing blossom! That is global warming!

As for Nails, well these are something that are almost entirely missed out from the physical examination findings , as nails are simply not looked at by most junior doctors.


I sometimes take a long time looking at nails, as they can sometimes give the diagnosis!

For example, Splinter Haemorrhages can signify endocarditis (more than 6 are significant). Clubbing can lead the physician to look for one of the many causes of this physical finding.

Moreover, finding Beau's Lines (a horizontal depression / line across the nail signifying nail growth arrest) can semi-quantitively date the time of the onset of the illness. The nails of the hand growth at 0.1mm/day = 1mm per 10 days. Hence, measuring from the line to the nail fold in millimetres and multiplying by 10 will provide the period of onset of the illness in days.

Nails can reveal the cause of a rare form of arthritis and a relatively common skin condition which include psoriatic arthritis and psoriasis respectively. For example, a patient may have a substantial thickening of the nail bed (subungual hyperkeratosis), the nail may become weak and break off from the nail bed (onycholysis), the nail may have many longitudinal lines and small 'pits' in the nail like a thimble used for sowing, so-called Nail Pitting.

Nails can reveal Aortic Regurgitation via Quinke's sign-- the in-out movement of blood in the interface between the white and pink areas of the nail due to the raised pulse pressure associated with this condition. It is quite rare to see it, but I have seen it 3 times in my career!!

Nail changes may also be seen in some inherited diseases such as the Polyendocrine Deficiency, Yellow Nail Syndrome etc....

Hence checking the nails can be a very important thing to do.

Clubbing-- should never be forgotten, but the causes cover many different systems.


Clubbing of a Patient's Fingers with Fibrotic Lung Disease















Cardiovascular

• Infective: Infective Endocarditis
• Genetic/Developmental : Cyanotic Heart Disease
• Cancer: Atrial Myxoma
  

Respiratory

• Infective: TB, Empyema, Lung Abscess, Pneumonia, Bronchiectasis
• Cancer: Primary Lung Cancer, Mesothelioma
• Inflammatory: Fibrosing Alveolitis / CFA
• Genetic: Cystic Fibrosis (from repeated suppurative chest infections)
  

Abdominal

• Inflammatory: Crohn's Disease, Ulcerative Colitis
• Malignancy: Lymphoma
• Metabolic: Chronic Liver Disease
• Malabsorptive: Coeliac Disease

Also Remember:

FAMILIAL (a friend of mine has congenital clubbing!!)

UNILATERAL CLUBBING:

• Axillary artery aneurysm
• Brachial arterio-venous malformations

Clubbing of a Patient's Toes!!






























My Normal Finger



Normal 'diamond-shape' when both index fingers are put together as mirror images. The diamond is normally produced but this diappears with Clubbing.

Examination....the wow factor

Many apologies for not writing in the last few days, but I have been busy in my teaching duties.

During my teaching at another hospital, I had finished going through the history and as a group we had made our way to see the patient.

I performed a basic but thorough physical examination and in a short time I had identified 5x splinter haemorrhages, left episcleritis and a mildly enlarged spleen.

The first year doctors seemed in awe that I had been able to find these problems.

The British medical teaching system concentrates from the very first year on how to examine the three main system and by then being fixed to different medical specialties, the student can learn the finer details of examination of each system.

As part of the final examination to become a doctor, some of it relies on being able to examine all systems to a certain level of competency and some doctors have been known to fail this part.

Later on, when the doctor wants to pursue higher level training he/she must revisit the very basic of examination skills and practise, practise and practise with the trainer being the Consultant doctors with each of them having their very own special technique of examining and with the learning doctor obtaining years of experience of the senior doctors in just a few months of training.

The higher level exams, in their final part, involve a very difficult physical examination test of 10 different scenarios which include:

• Cardiology
• Pulmonology
• Gastroenterology
• Short cases x2
  
• Opthalmology
• Neurology
  
• Rheumatology
• History taking
• Ethical discussion

Hence, the exam involves not only knowledge of diseases, but the doctor needs to show to the examiners that they can identify the disease without questioning the patient and just through physical examination. The exam also identifies whether the doctor is able to obtain a good history in the short time allowed, whether they can actually talk to patients and deal with problematic situations.

When I did the exam, it seemed like the longest 2 hours of my life with me sitting outside the various rooms and seeing other doctors going in and then coming out looking worried.... Only half the doctors are allowed to pass this exam and with the ones failing needing to retake several months later....I was the lucky one.

I have tried to continue the same high standard of examination skills that I was taught so that the junior doctors who I teach will have the benefit of my experience and as a result, they will have more confidence in making a clinical diagnosis.

In the end, once finely tuned, the complete 3-system examination from head to toe can be done in a very short time even in the outpatient setting.

So, when the junior doctors become enthused by my examining abilities, which to me seems quite usual, it makes me want to teach that much more!!

Thanks for your support!!!

Abdominal Pain and Collapse

This next case is a fascinating example of how CT scanning might have been helpful in establishing a diagnosis under these correct circumstances and indications. The case has been anonymised to safe guard patient confidentiality. This case is from the UK, not Japan, and is the unfortunate experience of a colleague of mine from several years ago.

Presenting Complaint

49 year old patient admitted with COLLAPSE

History of Presenting Complaint

He was normally fit and well and worked in a factory. Patient had been at pub in the afternoon when he stood up and suddenly collapsed to the floor. He lost consciousness for a few minutes only. Paramedics were called and patient was brought to the local ER department.

On arrival patient was grey in colour and sweating profusely and his T-Shirt was soaked with sweat.

1. Airway patent

2. Breathing- normal RR-16/min, SpO2 100% on oxygen via rebreath bag

3. Circulation BP 80/40 in both arms and pulse 100 beats per min and regular

GCS 15/15

Temp 37.5 Dry mucous membranes. Patient overweight

CVS: JVP not seen as patient had a large neck

Heart sounds 1 + 2 and normal. No added sounds / murmurs. No peripheral oedema

Resp: Percussion Resonant, chest clear, no wheeze / crepitations

Abdo: Soft , but epigastrium / peri-umbilical tenderness, No rebound / guarding, No hepatosplenomegally, Bowel Sounds present. Rectal- normal stool.

Central Nervous System: Pupils equal and reactive to light. All Cranial Nerves normal.

Peripheral Nervous System- tone, power, reflexes, plantar responses WNL.

ECG: Slight ST flattening in V5/V6 but no elevation/depression

CXR: Normal cardiac size. Nil acute.

Clinical Impression: Collapse with shock ? cause

Two intravenous lines inserted and fast IV fluid given. Urinary catheter placed— clear urine obtained.

Blood pressure improved to systolic of 100mmHg and pt was stabilized to be moved into observation area.

Now patient being more alert, he could answer more questions:

When he collapsed he was not sure what happened. He denied tongue biting / urinary incontinence / seizure and no seizure was witnessed by bystanders. He had slight abdominal discomfort only. No palpitations / no headache / no dizziness normally when standing.

No chest pain / neck-arm pain. No previous collapses in his life.

He admitted to recent diarrhoea and he had eaten mussels the previous evening but his wife and daughter had not eaten them. The mussels had been frozen and cooked in the microwave. He admitted to only one episode of diarrhoea. The abdominal pain was more of a discomfort but was not associated with any further diarrhoea. He felt thirsty. No blood in stool.

Previous Medical History: Nothing of note.
Medications: No regular drugs
Family History: Nil of note
Social History: Drank alcohol 2 pints/day, Non-smoker, Lived with wife and daughter in a house

Blood Results

Hb 13.4 Urine- NAD
WCC 12.4
N% 70%
Plts 300
MCV 82.3

CRP/ESR not tested

Na 134
K 4.5
BUN 28.8
Creat 1.58

Liver function tests normal

CK normal. Troponin-I WNL.

Arterial Blood Gas:

Metabolic Acidosis pH 7.31, low HCO3, BE -3, PCO2 low and normal PO2 on air.

Problem List

1. Collapse with shock

2. Abdominal Discomfort and Diarrhoea

3. Mild Renal failure

4. Metabolic Acidosis ? second to renal failure ? Lactic acidosis from organ hypoperfusion

5. History of sea food ingestion

Differentail Diagnosis

• Possible severe invasive GI food poisoning and volume depletion from diarrhea ? Salmonella infection/ E. Coli 0157:H7
  

• ? Ischaemic bowel

• ?? evolving Silent MI (only flattening of ST segment and normal CK and Trop I but maybe too early)

• ??? Aortic Dissection (normal CXR, no differential pulses but profound hypotension)

PLAN

1. Continued fluid resuscitation

2. Abdominal Xray

3. Stool culture

4. Antibiotic treatment with ciprofloxacin for ‘travellers diarrhoea’

5. Arrange CT thorax and abdomen: doctor had to speak with the Consultant On-Call at home to get pemission to do an 'out of hours' CT scan.
   

6. Close observation

Patient then moved to Medical Care unit

Blood pressure was stable and systolic improved to 120mmHg and urine output initially adequate.

The Hospital Doctor discussed the patient with the 'on-call' Consultant who was at home sleeping!—HOWEVER, the Consultant was not convinced from the history, physical and ensuing test results that the patient had an aortic dissection, so an emergency scan was refused!!

AXR- not focal abnormality detected.

Patient still complaining of abdominal discomfort and so the on-call hospital doctor re-examined. No changes evident from admitting examination.

Pulse was still tachycardic despite adequate volume filling and urine output then decreased to <20ml/hour. Patient was now complaining of feeling breathless.

Chest was re-examined and was entirely clear.

The On-call doctor then considered, however unlikely, that the patient may have sustained a Pulmonary Embolism as this may cause abdominal pain and dyspnoea.

Repeat ABG on air showed no hypoxia, but Metabolic Acidosis had worsened significantly pH 7.22, BE -10, low HCO3 and CO2. Normal PaO2.

Very soon afterwards, the patient then started to scream and became confused and I am told that he said 'I cannot breath, I cannot breath' and then he collapsed on his bed.

Cardiac Arrest Call was put out

Pt had a non-shockable rhythm and despite 30 minutes of intense cardiopulmonary resuscitation, he was unable to be revived.

What was the diagnosis???

On reviewing the history, data and clinical picture, the doctor considered that the patient may have had a severe type of food poisoning e.g. E.Coli 0157:H7 due to renal failure and shock with recent history of diarrhoea.

On the other hand, the on-call hospital doctor considered that however unlikely, with nothing else otherwise fitting the clinical picture, the patient may have developed an aortic dissection. But, how could this be?

This patient had none of the classical symptoms and signs of dissection. There was no history of chest pain, no interscapular pain and no pulse differential. The feeling of breathlessness may have been due to metabolic acidosis, but a metabolic acidosis does not give you ‘Air Hunger’. Kussmaul's respiration , as seen in a diabetic ketoacidosis, is however similar to air hunger but in this case, the pH of 7.22 was probably not low enough to give a severe Kussmaul's-type picture.

Air Hunger occurs when the patient has insufficient cardiac output to maintain normal respiration and is a sign of acutely impending cardiovascular collapse.

Did this patient have an acute cardiac tamponade and a distal dissection too? This would mean that there would have to be a large proximal-distal dissection with GI and renal arteries involved.

Plan

Post-Mortem was arranged through the local government investigative officer (known as the coroners officer whose legal duty is to investigate all unusual deaths) and Toxicology/Microbiology investigation

Post-mortem the next day—the On-Call doctor was in attendance.

Diagnosis: Cardiac Tamponade and Dissection of thoracic and abdominal aorta.

No major neck arteries had been affected. The pericardial sac contained approx. 500ml blood and the heart chambers were empty of blood. The Aortic Valve had a small tear and there was the classical fibrinoid changes seen in the dissection area. The Aorta was stripped by the dissection and there was a false lumen. The renal arteries had been affected too.

The On-Call doctor had been correct about the diagnosis and correct to inform his senior of his concerns about the suspicion of Aortic Dissection, but the Consultant, having not seen the patient himself, had simply not appreciated the extent of the patient's severity and had clearly made a error of judgement in refusing to allow for an emergency CT scan.

However, even if this patient had had an emergency CT scan, which would have probably been diagnostic of a Dissection, at this Hospital there were no Cardiothoracic Surgical Specialty services and he was too unstable to be moved to a Specialist centre in time for the extensive cardiovascular surgery that he ultimately required.

If the patient had have been scanned earlier, or if the Echocardiographic services had been available out of hours, then the diagnosis would have been confirmed much sooner, but again it is very unlikely that this patient could have been saved in time.

Clinical Gem From This Case:

If you consider dissection then it must be excluded. Dissection may not give chest pain and the Chest Xray may be completely normal initially, but it can present with sudden collapse and shock and abdominal pain. Metabolic acidosis in this case was probably due to organ ischaemia. The worsening renal failure over hours despite adequate fluid input and adequate systolic BP should be a cause of concern and warrant further investigation.

Quite clearly, the out of hours scanning services in the UK is insufficient to meet the needs of the patient and despite this hospital having a CT scanner and an MRI machine, the Consultant made an error of judgement in not allowing for an emergency scan. The UK hospitals have strict rules on who and who may not have an emergency CT/MRI scans but in some cases the refusal of such scans by senior doctors can prevent a diagnosis being made and a patient can suffer as a result. It would be better to see these rules relaxed somewhat and if not, then the Consultant should have got up from his bed to come and see the patient for himself....!

It would be useful for junior doctors to be taught the basic skill of ultrasonography / echocardiography, just like in Japan, as these non-invasive techniques can again give valuable information to the physician especially in emergency situations.

If you have any comments on the above then please let me know.

Amiodarone and Cardiac Dysrhythmias

Today's Blog is based on my own experiences in the treatment of cardiac dysrhythmias with Amiodarone.

My being one of the few physicians in Japan who has had experience of the use of Amiodarone (in UK patients) I hope the following will provide you with some 'hands-on' information about this drug.

When I have talked of Amiodarone in Japan I am always met with the same answer and that is Japanese patients do not want to take Amiodarone because of its side effects.

However, from my own experience, in treating many hundreds of patients with intravenous and oral preparations of Amiodarone in the UK, I have always found it to be a safe drug to use and occasionally there is the patient with amiodarone-induced side effects, but its benefits frequently outweigh its risks.

Amiodarone is usually prescribed for atrial fibrillation, but it is also used in the treatment of flutter, WPW, VT and VF.

The side effect profile includes asymptomatic corneal deposits, skin photosensitivity, slate grey discoloration of the skin (rare and with chronic use), thyroid dysfunction, liver dysfunction, pulmonary alveolitis and fibrosis, long QT/Torsade de Pointes, amongst others. However, it is a bit like reading the side effects of almost any major drug-- not all patients get all side effects and most patients get none of the serious listed side effects.

I have seen the occasional patient with thyrotoxicosis, pulmonary fibrosis and skin changes, but they are the exception rather than the rule.

I have seen many patients very effectively treated with this drug including a family relative who had Woolf Parkinson White Syndrome.

The other treatments for AF such as beta blockers, calcium channel blockers e.g. verapamil, are still effective drugs although they are not true chemical cardiovertors but rate limiting agents and both these class of drugs can reduce cardiac muscle contractility and function, which Amiodarone does not appear to do. Other drugs such as flecainide or propafenone (Class 1c) can be used in the setting of Acute AF treatment but flecainide cannot be used in patients with underlying ischaemic heart disease, unlike amiodarone, and both drugs used long term may increase mortality. Some Class 1a agents can also be used, but if toxicity occurs there can be pro-arrhythmic effects.

In the UK, in a patient with fast AF without cardiovascular compromise, unless contraindicated, in my opinion, most physicians would tend to use IV amiodarone infusion to rapidly slow the AF with an aim to chemically cardiovert the rhythm and oral therapy would then be instituted. Of course most physicians have their own personal preferences and sometimes use other drugs instead. If that fails, they would consider DC cardioversion if AF had occurred within 48 hours.

Amiodarone is usually continued in patients who do not initially cardiovert with concomittant anti-coagulation, and after 4 weeks, if there are no contraindications such as cardiac thrombosis on echocardiography, they would be electrically cardioverted. Amiodarone in conjuction with electrical cardioversion improves the cardioversion rate and patients can stay in sinus rhythm for longer.

In the UK Resuscitiation Council Guidelines over the past several years, Amiodarone has been included as the main anti-arrythmic agents to be used in VT or VF treatment rather than lignocaine/lidocaine. I have personally treated VT with Amiodarone and cardioverted patients without the need of electrical cardioversion.

The use of amiodarone can also coarsen VF from a situation of 'fine' VF making the rhythm more treatable by defibrillation.

As I am informed, at the present time, Japan has only just licensed the oral formulation of amiodarone last year but IV is still not available.

However, now that oral amiodarone is available, you now have a very effective drug at hand for the treatment of the very common cardiac problem of AF. From my own experience, and from reading the literature, this drug is regarded as safe when used correctly, and at a minimum maintenance dose of 200mg/day there should be minimal side effects.

Bear in mind that Amiodarone has a very long half life as it is very liposoluble and even on stopping such medication, the literature suggests that it may continue working for up to a year.

Always refer to your Japanese drug guides for directions when considering prescribing any new drug.

There are new agents that may be available in the next few years and these include purer Class III agents such as ibutilide, dofetilide and dronedarone, the latter being a deiodinated derivative of amiodarone which has no organ toxicity and a better side effect profile.

If you would like further information about my experiences with this drug then please write including your email.

Poisonings

Poisoning from drugs or toxic substances is a vast topic and to cover this in a blog would be impossible.

When dealing with poisonings it is necessary to establish whether ingestion was accidental or deliberate.

In my experience, deliberate ingestion is usually done by people wanting to committ suicide and sometimes, unfortunately, they succeed despite medical intervention.

When investigating an ingestion, one needs to establish the drug/s or toxin/s ingested, their dose or quantity and the time at which these agents were taken e.g. at the same time or staggered over hours or days.

In the UK, most overdose patients use acetaminophen which effects can take up to 48-72 hours before signs of acute liver failure ensue. Sometimes aspirin is also ingested and some of such overdoses are done under the influence of alcohol, which can worsen matters due to the combined toxic effects of such ingestions.

Hence, it is quite usual and proper to examine blood for these above agents even if the patient denies taking them or as part of an overall drug screen in the intoxicated patient. Tricyclic agents can also be tested for, as can urinary amphetamines / cannabinoids.

It is of prime importance to check for the above agents as treatment is available to reverse the associated problems caused in the early stages of ingestion.

For example, acetaminophen ingestion can be treated with iv n-acetylcysteine or oral methionone to reduce hepatotoxicity and renal injury and forced alkaline diuresis for aspirin overdose respectively. Activated charcoal can bind the tricyclic antidepressant agents plus many other drugs which can be inactivated by this method.

One very real example I saw and eluded to yesterday in my blog was of a female patient of 30 years old that I saw in the UK who presented with an overdose of Ethylene Glycol (EG) and alcohol. She presented with a decreased conscious level and her family had found an empty bottle of the EG around her plus it was noted she had been drinking Gin.

On admission her vital signs were stable, but conscious level was GCS reduced with the patient not eye opening, confused words and withdrawal to pain (E1 V4 M4 =9/15), pupils were 4mm each but unreactive. Reflexes were generally absent except for the triceps bilaterally. Babinski sign was uninterpretable.

Chest and abdominal examinations were normal.

Blood gas showed a pH of 7.1, pCO2 14, HCO3 3.8, BE -25, pO2 98.

Anion Gap 26

BUN normal. Creatinine 1.2, Na 134, K 7.0

Corrected Calcium for Albumin = 8.6

Liver function Normal.

WCC 28.8 but other blood elements normal.

Urine analysis - normal. No blood / protein / casts

With the Anion Gap being > 25 and a profound acidosis with a very low HCO3 <8,> methanol or ethylene glycol. Hence the blood results fitted with the history. However, the severe side effects of these agents are blindness or renal failure respectively.

The patient was given rehydration and bicarbonate and therapy for hyperkalaemia (see blog of yesterday)

By morning, her GCS had improved and she was able to open her eyes on command, follow commands and answer questions appopriately (GCS 14/15).


On reviewing the patient, it appeared that left flank pain was a new problem and the renal failure was now becoming worse with a rising BUN and creatinine. The K had normalised to 3.5. Calcium was still with normal limits.

It was suggested that the patient be given the Alcohol Dehydrogenase Inhibitor Fomepizole or iv alcohol to slow down the break down of the ethylene glycol. The former drug has a much better treatment profile and is easier to control with few side effects rather than the undesired effects of alcohol.

Moreover, the patient was given mulitvitamins such as folate, Vit B1 and Vit B12.

The concern about this patients kidneys made me concerned about ensuing renal failure from the formation of Calcium oxolate and other byproducts, which is the by product of EG breakdown through binding of free calcium.

Hence, when a patient is admitted poisoning, history can be extremely helpful although with a semi-comatosed patient such history will need to be taken from family or friends. Inviting such bystanders in to obtain information can provide a wealth of information and such people will feel that they have been empowered by the medical team and feel respected, and they are less likely to complain about YOU for the fact that they have been kept appraised of the information.

Physical examination may not be very helpful in these cases.

However, basic blood tests including an ABG, drug levels of common poisonous drugs plus blood chemistry can point the physician in the right direction.

One of the best texts I have found to date is UpToDate (www.uptodate.com) which is a paid subscription service to the most up to date of medical information including poisonings.

I would highly recommend this service.

All the best!