From Confusion to Coma: a Catastrophic Deterioration
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52 Postgrad Med J 2001;77:52–55 Postgrad Med J: first published as 10.1136/pmj.77.903.53a on 1 January 2001. Downloaded from SELF ASSESSMENT QUESTIONS From confusion to coma: a catastrophic deterioration K Ashkan, F Johnston Answers on p 56. A previously well 45 year old woman presented ventilated before transfer. On arrival at the to the local casualty department with a one day neurosurgical intensive care unit, she was history of generalised headache, neck stiVness, found to have bilaterally fixed and dilated and blurred vision. On examination she had a pupils, with no corneal or gag reflexes. There temperature of 38°C, a pulse of 80 beats/min, was, however, abnormal flexion of the left and a blood pressure of 130/80 mm Hg. Neu- upper limb. She was given mannitol and urgent rologically, she had spontaneous eye opening repeat CT was carried out (fig 2). An operation and was able to obey commands, although she was then performed, but postoperatively she had confused speech (Glasgow coma scale failed to show any clinical improvement and (GCS), 14). Pupils were equal and reactive died the next day. with no cranial or peripheral neurological defi- cits. Blood tests showed a raised white cell Questions count of 20.9 × 109/l with a neutrophilia (1) What does figure 1 show and what is the (19.2 × 109/l). Computed tomography (CT) of diVerential diagnosis? the brain was performed (fig 1), on the basis of (2) How does figure 2 relate to the change in which the patient was referred to the regional the patient’s clinical condition? neurosurgical unit. While awaiting urgent (3) Discuss the management of this condi- transfer, however, her clinical condition sud- tion. denly deteriorated. There was no eye opening or verbal response, although she flexed to pain- ful stimuli (GCS 5). She was intubated and http://pmj.bmj.com/ Department of Neurosurgery, Atkinson Morley’s Hospital, Copse Hill, Wimbledon, London SW20 0NE, UK K Ashkan F Johnston on September 30, 2021 by guest. Protected copyright. Correspondence to: Mr Keyoumars Ashkan, Department of Neurosurgery, Hurstwood Park Neurological Centre, Princess Royal Hospital, Haywards Heath, West Sussex RH16 4EX, UK Submitted 7 October 1999 Figure 1 Computed tomography of the brain at the initial Figure 2 Computed tomography of the brain following the Accepted 20 December 1999 presentation. sudden deterioration. www.postgradmedj.com Self assessment questions 53 Postgrad Med J: first published as 10.1136/pmj.77.903.53a on 1 January 2001. Downloaded from Cyanosis in late teens S G Williams, D J Wright, U M Sivananthan Answers on p 56. An 18 year old youth presented with a three year history of decreasing exercise tolerance and cyanosis. Physical examination revealed clubbing and cyanosis, with an estimated oxygen saturation of 76% (on air). There were no other abnormalities on cardiovascular or respiratory examination. Arterial blood gas Institute for Cardiovascular estimation revealed a PO2 of 5.85 kPa breathing Research, Yorkshire air, increasing only to 6.8 kPa after 10 minutes Heart Centre, Jubilee on 100% oxygen. Haemoglobin was 22 g/dl. Building, Leeds ECG, chest x ray, and conventional echo- General Infirmary, Leeds LS1 3EX, UK cardiography were normal. S G Williams A transoesophageal echocardiogram is D J Wright shown in fig 1. Figure 1 Transoesophageal echocardiogram. Ao, aorta; U M Sivananthan LA, left atrium; MPA, main pulmonary artery; RPA, right pulmonary artery. Correspondence to: Questions Dr Williams (1) What is the most likely cause of the cya- [email protected] nosis? Submitted 5 November 1999 (2) What does the transoesophageal (3) What treatment options are available for Accepted 31 January 2000 echocardiogram show? this patient? Recent onset of bleeding and gross coagulopathy R E Hough, M Makris http://pmj.bmj.com/ Answers on p 57. A 58 year old unemployed man was admitted Clinical chemistry—creatinine 113 µmol/l, as an emergency with a two week history of glucose 5.0 mmol/l, adjusted calcium 2.35 gum bleeding and a one day history of gross mmol/l, aspartate transaminase 17 U/l, alanine haematuria. Other than osteoporosis and low transaminase 18 U/l, bilirubin 5 µmol/l, ã back pain his past medical history was glutamyl transferase 45 U/l, albumin 39 g/l. unremarkable. He had had previous dental extractions and major surgery without any on September 30, 2021 by guest. Protected copyright. excessive bleeding. He did not have a family Coagulation tests: history of a bleeding disorder. His diet was + Prothrombin time 230 s (normal range normal and contained vegetables and fruit. His 9.5–11.5 s). weight was stable, his appetite was good, and + International normalised ratio (INR) 25.5. he had no bowel symptoms. Regular drug + Prothrombin time + 50% normal plasma ingestion was confined to co-codamol, Distal- 9.5 s. Department of Haematology, gesic, and diazepam. His alcohol intake was + Activated partial thromboplastin time Royal Hallamshire less than 10 units/week. Clinical examination (APTT) 116 s (normal 27–36). Hospital, was unremarkable and he had no purpura or + APTT + 50% normal plasma 49.3 s. Glossop Road, echymoses, no hepatosplenomegaly, and no + Thrombin time 18.6 s (normal 18–23). SheYeld S10 2JF, UK signs of chronic liver disease. R E Hough + Fibrinogen 7.7 g/dl (normal 1.7–3.3). M Makris INVESTIGATIONS Correspondence to: His blood test results on admission were as fol- Questions Dr Makris lows: (1) What is the diVerential diagnosis? [email protected] Full blood count—haemoglobin 14.7 g/dl, (2) What is the most likely diagnosis and how 9 Submitted 28 October 1999 white cell count 12.5 × 10 /l, platelet count would you prove it? Accepted 22 December 1999 222 × 109/l. (3) How would you treat this patient? www.postgradmedj.com 54 Self assessment questions Postgrad Med J: first published as 10.1136/pmj.77.903.53a on 1 January 2001. Downloaded from A young man with seizures, abusive behaviour, and drowsiness A G Unnikrishnan, S Rajaratnam Answers on p 58. A 20 year old man was brought to hospital with progressive drowsiness and vomiting for three days. Two weeks before admission his relatives noted that he was becoming agitated, violent, and abusive. He had previously fractured his left humerus owing to a fall during a seizure. He had been on phenytoin and phenobarbitone for seizure control for the past two months. There was no history of substance abuse or alcohol intake, neither was there a history of previous neck surgery. On examination he was dehydrated and he had a tachycardia, a low blood pressure (90/70 mm Hg), and low central venous pressure (+4 cm). He was found to be talking irrelevantly and not obeying commands. He had general- ised rigidity. There was no papilloedema. Systemic examination revealed no other abnor- Department of mality. Figure 1 Computed tomography of the brain. Endocrinology, CMC Haematological investigations were normal. Hospital, Vellore—632 Serum biochemical investigation results were parenchymal lesions. Computed tomography 004, Tamil Nadu, India as follows (mmol/l unless stated): sodium 130, of the brain is shown in fig 1. A G Unnikrishnan potassium 3.6, bicarbonate 13, chloride 105, S Rajaratnam magnesium 0.53, calcium 1.025 (corrected Questions Correspondence to: calcium 1.36), phosphorus 1.81, albumin 23 (1) What is the diagnosis? Dr Rajaratnam g/l, urea nitrogen 38.1, creatinine 318 µmol/l, (2) What factors could have worsened the [email protected] and intact parathormone (PTH) 2.1 pmol/l hypocalcaemia in this patient? Submitted 26 October 1999 (normal 1.3 to 7.6 pmol/l). Ultrasound of the (3) What is the diVerential diagnosis on the Accepted 22 December 1999 abdomen showed normal sized kidneys with no computed tomograph of the brain? http://pmj.bmj.com/ A case of reversible amnesia J Stone, I W Campbell, G D Moran, C J Mumford on September 30, 2021 by guest. Protected copyright. Answers on p 59. A 43 year old, normally healthy woman was days of intravenous acyclovir for a presumed admitted to a general medical ward after generalised seizure possibly complicating viral Department of Clinical collapsing at home. Over the preceding two encephalitis. Subsequently, CSF and serum Neurosciences, weeks, her husband had noticed that she had viral serology and an autoantibody screen were Western General Hospital, Edinburgh seemed distracted, unusually depressed, and negative. EH4 2XU, UK “not herself.” He had found his wife unrespon- During and after treatment she had a fluctu- J Stone sive and writhing on the floor. She was initially ating level of confusion and appeared distant G D Moran drowsy after the attack but became alert within with a flat aVect. Three weeks after the initial C J Mumford 30 minutes. On admission, she was amnesic for presentation she had another episode of the episode, disoriented in time, place, and collapse with writhing movements as before. Department of Medicine, Victoria person, apyrexial, and clinically euthyroid, with Her mini-mental state examination was 19/30, Hospital, Kirkcaldy no meningism or focal neurological signs. with deficits in orientation and attention and and Department of Computed tomography of the head was total anterograde amnesia. Her neurological Medical Sciences, normal. CSF protein was 0.74 g/l (normal examination remained otherwise normal. She University of range 0.35–0.45 g/l), with normal glucose and was still clinically euthyroid. Her TSH had St Andrews, Fife, UK I W Campbell no cells. Serum biochemistry and full blood increased to 25 mU/l with a normal T4 of 15 count were within normal limits, apart from pmol/l. Her thyroid microsomal antibodies Correspondence to: her thyroid stimulating hormone (TSH) which were raised at more than 1:6400.