Chapter 5: Sinister, deadly and not to be missed

The following case history is a medico-legal case where I was requested to write a report and one of many where I experienced that gut-wrenching feeling of ‘there but for the Grace of God go I’.

‘Sarah’, aged 3 years, attended a general practice one evening because she was unwell, lethargic, febrile, refused to eat and had developed a fine macular rash on her trunk. The examining practitioner noted that she was lying quietly, looked pale and had the pink rash on her chest and back. The only recorded vital sign was a temperature of 38.5 °C (otic).

A diagnosis of the viral infection, roseola infantum, was made, paracetamol prescribed, and the parents were advised to return or contact him if her condition deteriorated. Sarah did deteriorate with drowsiness, floppiness, cold extremities, breathing difficulty and a change in the rash to ‘black’. Her parents took her to the nearest main hospital where she was admitted with meningococcal septicaemia. After a lengthy stay she did survive but had to have partial amputations of both arms because of severe ischaemia.

There are many reported cases of children and adults deteriorating and dying with or without prior consultation. The court proceedings were prolonged and harrowing for all concerned. The judge was particularly critical of the GP for failing to record all the vital signs in the history—temperature, pulse rate, blood pressure and respiratory rate.

Chuck was a 55-year-old American general practitioner who was our house guest for a few days. Arriving in Australia for a holiday, he commenced his journey to Melbourne from Cairns in a rented motor home. When he arrived he said that the long trip on unfamiliar roads was so stressful that he had resorted to chain smoking. He said that he had a history of angina pectoris and was taking glyceryl trinitrate by pump spray for any chest pain. He retired saying that he felt more relaxed and was looking forward to a good night’s sleep.

At midnight we heard a commotion in the upstairs bathroom where we found a deathly pale, vomiting and sweating Chuck with chest pain and classic angor animi. He was terrified and using his glyceryl trinitrate spray indiscriminately.

It was obvious that he had suffered a myocardial infarction and looked as though cardiac arrest was imminent. We rang for the MICA ambulance and gave him soluble aspirin. The ambulance arrived in about 10 minutes and performed an ECG which showed an anterior infarction and then transported him to the nearby major hospital. His wife informed me that he had taken Viagra and was having sex when the pain struck.

When he arrived at the hospital emergency department after a fast 15-minute trip he had a cardiac arrest and was successfully resuscitated with defibrillation. He was then whisked off to the coronary catheter laboratory where he had a stent placed in the left anterior descending artery. When we visited him nine hours later he looked well, as though nothing dramatic had eventuated during the night.

CASE 1

‘Will you come down to the hospital to see yet another football player? He doesn’t look too good. Probably has broken ribs and pneumothorax.’.

‘Typical Saturday afternoon’, I thought as I went to see Robert S, aged 22. Robert was holding a painful precordium and looking pale and sweaty. ‘Did you get a heavy knock?’ ‘No, not really.’ His chest was normal on clinical examination. ‘If he was older I’d think it was myocardial infarction’, I thought just before he moaned loudly and then collapsed.

Resuscitation, despite optimal facilities, was unsuccessful. Autopsy showed acute myocardial infarction (AMI).

CASE 2

Lila J, aged 62, was the local Methodist minister’s wife, a truly beautiful person who attended me for hypertension. One evening I was called to her home because I was told: ‘Mum is complaining of a funny constricting feeling in her throat and is having trouble breathing. We’ve had fish for tea and we think she must be allergic to it’.

I hurried to treat the acute allergic problem, only to find a very pale and anxious-looking lady who said, ‘My throat is tight and closing up’. As I nervously felt a slow and irregular pulse, she had a cardiac arrest.

To the horror of the onlooking loved ones, I commenced cardiopulmonary resuscitation and asked one of the relatives to bring in my portable defibrillator. This was successful initially but she died some time later in hospital.

CASE 3

Alan P, aged 49, is a mountain of a man who uses jackhammers each day as he drills through concrete. He presented one afternoon looking quite well but claiming, ‘This work is catching up with me—I’ve had terribly aching arms all day’. Further questioning revealed that he had the pain in both forearms for five hours and then reluctantly came in when he felt ‘lightheaded and peculiar’. I could find nothing abnormal on examination but intuitively took blood for cardiac enzymes and performed an ECG—another AMI.

CASE 4

Mary B, a 41-year-old housewife, presented with the sudden onset of severe pain in the interscapular area of her back. However, I could find no abnormality on examination of her thoracic spine. My provisional diagnosis included a pathological fracture in an osteoporotic vertebra, but a routine ECG provided the answer to the unusual presentation—AMI and not a twinge of discomfort in the anterior chest.

CASE 5

I was called to see Sarah C, a 72-year-old diabetic, at 3 am because of the sudden onset of dyspnoea. ‘An easy one’, I thought as I sped to the farmhouse. ‘Morphine, frusemide and oxygen will fix her acute pulmonary oedema in no time. Love treating them.’ Well, that treatment did not make any impression on her distress (anxiety, sweating, dyspnoea). Unfortunately, she died in hospital from the complications of her AMI. Never a complaint of chest pain—a truly silent AMI that precipitated acute cardiac failure.

CASE 6

A first-aid person rang me one afternoon to say that 78-year-old Minnie P had been run over by a car in the main street of the town. ‘She’s in bad shape—multiple fractures, ribs and left humerus at least.’.

My first sighting in the casualty area was a ‘shocked’ elderly lady with abrasions who was moaning with pain. She pointed to her sternum, precordium and left arm. There was no clinical evidence of fractures. I quickly organised an ECG, which confirmed AMI. Minnie died two hours later. The attending policeman said, ‘The driver had been let off the hook. He was emphatic that she suddenly fell onto the road and then under the car as she was crossing it in front of him’.

CASE 7

Phyllis M, aged 62, a close relative of the author, requested another opinion about severe epigastric pains and ‘indigestion’ diagnosed as a peptic ulcer but unrelieved by antacids and H² antagonists. It was a real brain teaser, but her obvious pallor and discomfort prompted an ECG, which confirmed a recent AMI.

CASE 1

Betty R was a 68-year-old housewife and ex-nurse living in retirement in a pleasant rural area when she presented for a general check-up. She claimed to be in good health but had been bothered slightly by ‘sluggish bowels’ and vague abdominal discomfort for the past year or so. She had a long history of mild hypertension for which she was taking low-dose beta blockers. She was a very matter-of-fact ‘now you see her, now you don’t’ type of person who conveyed the impression that she felt that she was bothering her doctor and wanted to get on her way with her script.

During this particular consultation I sensed that she was ready for some dialogue and perhaps reassurance. Fortunately, I asked that marvellous question, ‘Do you have any particular concerns about your health?’.

‘Yes’, she said, reflectively yet urgently. ‘I am the only surviving member of my family. They all seemed to die mysteriously around the age of 70. I remember that my father died quite suddenly. He was in great pain and went very pale. No one seems to know what he died from—it was very strange, no post mortem was done. They thought it was a heart attack. My sister, who lived alone, was found dead in bed although she had been quite well the previous day. She had cancer of the breast, but her death at 65 years was sooner than expected.

‘The death of my brother at 69 about 6 years ago really upset me. He was in the country and developed severe pains in the back and stomach. He was rushed to a city hospital but was dead on arrival. I don’t know what he died from.’.

DIAGNOSIS

This challenging history fascinated me and obviously caused Betty considerable anxiety. Her brother’s history started me thinking about ruptured aneurysms of the abdominal aorta, and knowing the familial history of such lesions I directed my physical examination carefully towards the abdomen.

Abdominal palpation revealed the characteristic pulsatile mass of an abdominal aneurysm, which I estimated at about 50 to 60 mm.

Betty had been unaware of the presence of an abdominal mass, but said she felt that something had been wrong with her stomach because it ‘felt tender and uncomfortable at times’.

I reassured her that we had discovered the probable cause of the family malady and that her outlook was fine. I organised an ultrasound examination, a referral to a vascular surgeon and wrote to Flinders Medical Centre for details about the possible cause of death of her brother.

THE OUTCOME

Ultrasound examination showed an aneurysm about 60 mm in diameter. I eventually found out that her brother had died from a ruptured aneurysm of his abdominal aorta.

Betty underwent surgical repair three weeks later. The surgeon was alarmed to find ‘a paper-thin wall to the diseased vessel’ and one can only speculate on how inevitable a rupture would be. Despite the setback of a pulmonary embolus, Betty is now fit and well and ponders over her good fortune, but she worries about her seven children now entering middle age.

CASE 2

Eric P was a fit 59-year-old bus driver who presented to me for a check-up and discussion about his family history. His father had died suddenly aged 62 from a ‘heart attack’, and a brother had also died suddenly at 60 from a ‘heart attack’ and yet another surviving brother who was a smoker suffered a ‘heart attack’ at 56 years. A common feature was the suddenness of the myocardial infarction without any preceding angina or other ill health.

Eric had been so aware of this poor family history that he had been meticulous with his health and lifestyle. He kept fit and trim, followed a strict diet, did not smoke or drink and practised relaxation.

Physical examination, chest X-ray and an ECG revealed no abnormalities. In particular his cardiac function and blood pressure were normal. I organised a stress ECG test that provoked some chest discomfort typical of angina at high stress. Ischaemic changes were noted on the stress ECG.

I decided to refer him to a cardiologist for further evaluation. About 10 days later while awaiting his appointment (due in four days’ time) he suddenly collapsed. He was dead on arrival at the hospital.

It was one of those occasions in the life of an overworked country doctor when the impending arrival of the locum produced visions of relaxation in a subtropical resort. The ringing of the phone jolted me back to reality. An anxious farmer informed me that his wife had suddenly developed an agonising pain in the middle of her back, which had persisted for an hour.

The inevitable thoughts sped through my mind as he spoke: ‘Another back problem. Surely it will subside. The locum can handle it. Well, it sounds unusual—rather like the old dowagers who suddenly collapse their osteoporotic vertebrae. Faye is young, trim and healthy—what could it be? What if it’s a dissecting aneurysm? Perhaps I should see her immediately’.

I saw an agitated Faye (42 years old and previously healthy) at the hospital 20 minutes later and found that she still had pain between the shoulder blades at the T4-T5 level. There was no anterior chest pain, nausea, dyspnoea or any other symptom. On examination there was absolutely nothing abnormal: no pallor, no inequality of the pulses and no spinal tenderness. The hypotheses continued to flow: ‘Could she have an acute disc prolapse? They are epidemic here in the bush. What about myocardial infarction? That is really a master of disguise and I saw a similar case five years ago. Time for an ECG’.

The locum arrived as I was performing the ECG in Faye’s hospital room and he confirmed my assessment of a normal tracing. We discussed the differential diagnosis and the management plan, which included an intramuscular injection of pethidine, hospitalisation and an X-ray of her thoracic spine.

DIAGNOSIS

The pain soon settled and, apart from general weakness, Faye was quite well until two days later when she suddenly developed twitching of the right side of her face, dysphasia, blurred vision and hemianaesthesia of her right side. This dramatic two-hour long episode provoked a phone call to a neurologist who arranged her admission to a city hospital. Several investigations including a skull X-ray, electroencephalogram (EEG) and a brain scan were performed, and all were negative. A diagnosis of anxiety and depression was attached to the patient who was discharged with a ‘magic remedy’—amitriptyline.

Faye consulted me on the first day after my holidays, and she complained of extreme fatigue and light-headedness. She appeared listless and pale, but the only abnormalities on physical examination were an irregular pulse and crepitations at both lung bases.

Further investigations

A repeat ECG showed evidence of an anterior myocardial infarction with ventricular ectopic beats. A chest X-ray and haemoglobin estimation were normal.

She had had a myocardial infarct after all. The cerebral ischaemic episode was caused probably by an embolus from a left ventricular thrombosis associated with a transmural infarct. (Using serial two-dimensional echocardiography, Asinger and his co-workers (1981) have demonstrated that left ventricular thrombus can develop 1 to 11 days after an acute transmural anterior infarct.).

The subsequent deterioration in her health with a cardiac arrhythmia (ventricular ectopic beats) and mild congestive cardiac failure was probably related to the tricyclic antidepressant.

Anne W was the vivacious 32-year-old kindergarten teacher of our children and also a personal friend. At 5 am on Easter Saturday I received an urgent call from her shaken husband to come to see her at their country school residence. Upon arrival some 20 minutes later, I found the glamorous Anne sitting up in bed saying, ‘I don’t know what all the panic is about—I feel fine now’. Her husband said, ‘Anne woke me calling out with severe stomach pain. She looked pale and dreadful—frightening’. Anne said that the pain in her lower abdomen lasted only 10 to 15 minutes. ‘I’ve been having trouble with my periods—bleeding when it shouldn’t— I think I need a change of the pill. I’ve made an appointment to see you on Monday.’.

After palpating a normal-feeling abdomen I was about to perform a pelvic examination, but the body language in that bedroom said, ‘Don’t touch—I’m comfortable—Don’t embarrass all of us with an internal’. So ‘chicken doctor’ flew back home.

DIAGNOSIS AND OUTCOME

On Easter Sunday I was called out of church. It was Anne. ‘Flat as a tack,’ said her neighbour, ‘I think she’s carked it. You’d better come quick’. ‘Bloody ectopic’, I thought as I sped off. ‘I dismissed it yesterday. She’s on the pill. Why didn’t I do a pelvic examination?’.

I arrived to find a semicomatose woman, of a similar colour to the sheets in which she lay, looking quite moribund. A quick cut down onto the cephalic vein and then intravenous Hartmann’s solution followed by Haemaccel brought an encouragingly rapid response with her blood pressure rising from 50/30 to 90/50. I sent her husband with a sample of blood for typing and cross-matching on the long trip to the base hospital to get blood, and then I transferred her to our bush nursing hospital. At surgery her abdomen was full of blood from the ruptured ectopic pregnancy. Once the bleeding was arrested and the transfusion commenced, the drama subsided.

During the ward round the following morning the glamorous Anne sat up in bed with make-up and bedwear fit for a film star. ‘Someone’s saved my life. I feel fine now’, she said. And all without a vaginal examination, I mused.

Sue T, a 27-year-old mother of two, consulted me 24 hours before admission to hospital for the biopsy of a breast lump detected three weeks previously. She described 19 days of painless vaginal bleeding beginning with the previous menstrual period. She interpreted this as a prolonged period related to the stress of the pending breast surgery.

Twelve months ago I had inserted a Copper 7 intrauterine device (IUD), which had proved very satisfactory apart from an occasional heavy period. She had not missed a period. I informed her that the persistent bleeding was probably due to the IUD, which should be removed. I could not remove it in the surgery because I could not locate the string.

I arranged that the surgeon would remove the IUD and perform a dilatation and curettage (D and C) during the breast biopsy procedure. He reported that the uterus seemed slightly enlarged but that no masses were palpable. She returned to me 10 days later complaining of lower abdominal pain for seven days, worse on defecation and micturition, persistent minimal vaginal bleeding and dyspareunia. Pelvic examination revealed a slight enlargement of the uterus and tenderness in the left fornix and Pouch of Douglas.

I arranged an appointment with a gynaecologist the following day, but her husband phoned me two hours later to say that the pain was now intense and that she had virtually ‘collapsed’. She was admitted to hospital immediately and the gynaecologist performed a laparoscopy, which confirmed an ectopic pregnancy of about six weeks’ gestation in the left Fallopian tube. Salpingectomy was then performed.

CASE 1

One evening I was called to our local hospital to an emergency. When I arrived I found a comatose and cyanosed 14-year-old lad who was beyond resuscitation. I recognised him as an asthmatic patient whom I had not seen for some time. According to his distressed mother, his asthma had been getting worse recently and had culminated in this fatal attack.

The mother explained that the family were unhappy about him inhaling ‘cortisone’ and drugs that make the heart race, and they sought the help of a naturopath who claimed that he could cure asthma. The patient then stopped his prescribed medication and underwent ‘herb and vitamin therapy’ as well as spinal manipulation. This sad occasion was not the time to pass comment about such treatment.

CASE 2

Dennis W, aged 22, attended one of my adult asthma education groups that are open to the public. He said that he had been self-medicating with salbutamol inhalers all his life.

I lent him a peak flow meter to accurately assess his respiratory function. The readings were unacceptable to both of us. He agreed to commence inhaled corticosteroids, and the improvements in his asthma (Figure 5.1), general health and morale were amazing.

CASE 3

Margaret M, aged 67, had late-onset asthma that showed unacceptable control. In fact the medication seemed to make little difference. I organised peak flow readings and studied her inhaler technique. The latter was faulty. We could not seem to correct her technique and so we introduced a spacer.

The change in her asthmatic control was dramatic and she has achieved a greatly improved quality of life.

Kate M, the 35-year-old wife of a teacher, made a striking impression when she first consulted me in my country practice. A beautiful person with a vivacious personality, she presented presumably for a prescription for a tranquilliser because of an ‘anxiety state’. When the consultation appeared terminated she casually mentioned: ‘Perhaps you should check my breasts. I had them checked a month ago by my previous doctor who said they were healthy but required “watching”’. A rather hurried examination revealed large heavy breasts with diffuse fibroadenotic thickening, the left breast lumpier than the right. Pinning excessive faith on the judgment of her previous practitioner, I concluded that they seemed okay but should be reviewed in six months. Breast self-examination was discussed. No imaging was available then.

Three months later Kate presented with a trivial complaint and again said: ‘Perhaps you should check my breasts before I go’. As I looked at the breasts I suddenly felt nauseated and tremulous as I could see skin dimpling over the left breast. A hard mass was tethered to the skin.

Three days later the surgeon phoned to confidently prognosticate: ‘It went well—we got all of the tumour—there were no involved nodes—stage 1—no further treatment will be necessary’. This news helped alleviate my guilt and embarrassment as I relayed the information to her husband who had posed the obvious question: ‘How come you guys didn’t pick this up beforehand?’.

Four months later Kate presented with a small hard lump in the scar and the ‘nightmare’ started. Carcinoma! X-ray therapy—another lump—cytotoxic therapy—extreme nausea, syncopal attacks, alopecia totalis—corticosteroid therapy—Cushingoid features—depression—multiple somatic complaints. She grew grotesque while deteriorating medically, and I wished that the stupid cytotoxic torture had never started. I felt bad—really bad. My guilt became sublimated into zealous caring, manifested in many impromptu home visits.

On one occasion she complained of an aching right thigh. Examination was quite normal so I reassured her it was probably ‘muscular’ and nothing to worry about. Two days later she was found lying on the kitchen floor with a fractured femur caused by a pathological fracture through a metastatic deposit in the femoral shaft.

Several days later I was called urgently to the hospital where she was convalescing from the insertion of a Küntscher nail by an orthopaedic surgeon. Kate was dead, less than 12 months after the initial consultation. She had called for a bed pan as a pulmonary embolus swiftly and kindly terminated the medical ‘merry go round’.

Mrs F, aged 53, presented with a four-week history of altered bowel habit, having diarrhoea and unsatisfied defecation. Her symptoms had begun about two weeks after a very pleasant four-week trip to South-East Asia. She felt quite well and had a normal appetite. There were minimal abdominal cramps and her stool was abnormal; on one occasion she had observed blood and mucus.

A full blood examination, microscopy and culture of the stools ordered at this visit revealed an eosinophilia, an ESR of 45 mm and also cysts of the parasite Giardia lamblia in the stool. The patient was given a course of metronidazole.

On review one week later her bowel actions were improved. A repeat course of metronidazole was prescribed and a full blood examination was performed two weeks later. This revealed no eosinophilia, and ESR was 15 mm. She was told to return in four weeks if her bowel actions were not completely normal. She did, complaining of further symptoms—the passage of mucus with flatus and the occasional sensation of prolapse of the bowel on defecation.

DIAGNOSIS

A rectal examination revealed a mass with a heaped margin at the tip of the gloved finger. Sigmoidoscopy confirmed a large annular ulcerated mass at 9 cm, which was bleeding. Biopsy demonstrated adenocarcinoma and an anterior resection was performed. Incidentally, the patient had a strong family history of carcinoma of the bowel.

The patient, a very sprightly 79-year-old woman, rang on Monday morning complaining of a sore throat and asked for a home visit. She usually walked the kilometre from her home to the surgery for checks on her blood pressure and asthma status and so I knew she was ‘genuine’.

When I was at the bedside, she complained of pain in the mouth and on the left side of the face. On examination she looked unwell and the left parotid duct orifice was swollen and oozing saliva. The provisional diagnosis was parotid duct calculus with superimposed infection, and appropriate treatment was commenced. Unfortunately, during the afternoon she became unsteady on her feet and fell twice, hurting her neck.

On review the next day she was a little worse; examination of the buccal cavity was limited because she found it difficult to open her mouth fully. Her neck was tender with considerable muscle spasm and she complained of cramps in her left leg. It was considered wise to admit her to hospital for further investigation and nursing care because she lived alone.

The specialist surgical opinion sought in the hospital agreed with the likelihood of a parotid duct calculus, but full blood examination and X-ray of the parotid region were normal. The diagnosis first occurred to me that afternoon, and after rejecting it a dozen times in my mind I broached the possibility, almost self deprecatingly, to the surgeon who felt it was possible, albeit rare.

DIAGNOSIS AND OUTCOME

The charge sister rang early the next morning to say that the patient was breathless—could I come to see her? On examination she was perspiring profusely and was having a mild to moderate attack of asthma. When on my suggestion she attempted to use her bronchodilator inhaler she could barely open her mouth wide enough to insert the mouthpiece.

Becoming bolder (after reading the relevant chapter in Harrison’s Principles of Internal Medicine (Isselbacher et al., 1991) and after further consultation and examination by a specialist physician—who felt the diagnosis was possible but uncertain—she was transferred to the infectious diseases hospital. Later that night she experienced further and more severe tetanic spasms, and was intubated.

Despite suffering a myocardial infarction in the ensuing weeks, she has survived her brush with tetanus and, after three months in hospital, is almost back to her former sprightly self.

It was a balmy April afternoon and outside a thick pall of smoke from the burning bush hung lazily in the autumn sky. Suddenly, the tranquillity was disturbed by the urgent screeching of brakes from a Forests Commission four-wheel drive vehicle at the surgery door. Two brawny foresters burst into the waiting room supporting their stuporose mate by the arms.

‘Doc, we thought that you should give Mick ‘ere a check-up. He seems to have one hell of a hangover but it’s getting worse. He’s vomited blood twice and he’s staggering all over the place.’ These hard-playing boys had seen it all before.

A very drowsy 20-year-old Mick then laboriously explained his problem. The previous evening he had been drinking heavily and playing cards with his mates in their mountain bush shack. This morning he had felt wretched with nausea, tiredness and headache when he started to burn off the low bush in the eucalypt forest. During the lunch break he felt worse: pains in the legs and abdomen, excessive sweating, severe nausea and headache. He received little sympathy from his workmates who berated him for his intolerance of alcohol.

He rested during the afternoon but still felt as if he ‘wanted to die’. After he had vomited blood twice and complained of blurred vision, his colleagues dumped him in the Land Rover and headed in my direction.

On examination he was pale, very weak and stuporose. His pulse was 90, with weak volume. BP was 95/60. There was mild abdominal tenderness but no guarding. A neurological examination of the cranial nerves was difficult; no specific abnormalities were detected. There was some voluntary muscular weakness but his reflexes were intact. During the examination he coughed up a moderate quantity of blood-stained mucus.

DIAGNOSIS AND OUTCOME

A provisional diagnosis of tiger snake envenomation was made. Mick could not recall having seen any snakes nor remember being bitten, but the undergrowth was waist high and he had felt many scratches and stings from the dry bush as he ran through. Specific examination of the legs revealed the telltale evidence of a snake bite: two small puncture wounds with a slight ooze of unclotted blood halfway up the right leg.

He was admitted immediately to the local bush nursing hospital (Figure 5.2.) We gave him an intravenous infusion of saline, added 25 mg of promethazine and then infused 3000 units of tiger snake antivenene, keeping a syringe with 1 mL of 1:1000 adrenaline nearby.

Mick was very weak and ill for three to four days. During the next six months he battled with a severe depressive illness. His relatives and friends claimed he was a completely different person, complaining of fatigue, multiple somatic complaints and an inability to work. He was weepy and suicidal. Fortunately, his recovery was complete albeit 2 years later.

The status of ‘doctor’ within a family especially an extended family brings many requests for help which at least can be a learning experience especially from the ‘cautionary tales’ perspective. One such case was that of first cousin ‘Mary’ who sought advice about a persistent ‘irritable bowel syndrome’. The condition had been present for 18 months and she had several visits to at least two doctors in the clinic. She had presented with vague lower abdominal discomfort. She found any pressure from clothing on the abdomen to be tight and uncomfortable. Throughout this period she gradually became flat and unwell and prone to episodes of constipation and diarrhoea. The diagnosis of irritable bowel syndrome seemed logical.

In recent weeks she had become anorexic and noticed weight loss. I was very concerned but did not want to interfere with her management so I suggested that she make an appointment with her GP as soon as possible. She was ordered an ultrasound and tumour markers which suggested carcinoma of the ovary. A laparotomy confirmed the presence of a large tumour causing tethering of pelvic structures. Surgery was eventually performed followed by chemotherapy. Despite a poor prognosis Mary is coping well after three years but, like so many having cytotoxic therapy, remains afflicted with the cold burning feet of peripheral neuropathy.

The following potpourri of cases from GP colleagues highlight the fact that warfarin is a major cause of threats to patient safety.

Mr JP, aged 78, presented with a large mass in the left hypochondrium after taking a double dose of warfarin. He was admitted to hospital with a provisional diagnosis of a splenic haemorrhage but he was found to have a haematoma of the rectal sheath. He seemed to have little understanding of warfarin action, dosage and monitoring. Mrs GL, aged 80, who was taking warfarin for atrial fibrillation, was prescribed an NSAID by a specialist for pain management. A rapid rise in her INR followed with haematemesis and melaena from gastric haemorrhage leading to a fatal outcome despite multiple transfusions.

Mr IT, aged 80, was discharged from the surgical hospital on warfarin for a pulmonary embolism following treatment for a fractured hip. He then spent 20 weeks in a bush nursing facility and base hospital before going home. When reviewed he was taking warfarin 2 mg bd as directed on the bottle from the original hospital. Both patient and family were confused. His INR was 4.5.

Ms AH, aged 58, who presented with rectal bleeding, was taking warfarin 5 mg daily for atrial fibrillation. Her INR was 11.0. She had spent four weeks interstate and missed her INR-warfarin monitoring by her regular GP. Luckily she settled without incident.

Mrs ML, aged 57, was admitted to hospital for a transient ischaemic attack and was discharged after warfarin was commenced. The following day she presented with a large haemorrhagic area on her right thigh. It became necrotic and then we battled to treat the ulcer for several months. It was a localised thrombosis apparently related to protein C deficiency and a large loading dose of warfarin.