Friday, 16 February 2007

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


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.

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