Chapter 7: Red faces

My young medical colleague in a city practice had just completed writing a pad prescription for an oral contraceptive for a young woman who infrequently came to the practice. My colleague noted that she had not had a Pap smear for three years and she willingly agreed that in the presence of the practice sister she would have one now. My young colleague went to fetch the sister and noted that a 20-year-old man was having an unusual type of convulsion on the floor of the waiting room. He administered necessary first aid to the young man, who then stood up and seemed perfectly lucid and well. My colleague’s Pap smear lady suddenly rushed from the examination room where she had been left on the couch during this man’s alleged convulsion, grabbed him by the arm, dashed out of the door and was never to be seen again.

Two hours later, two separate pharmacists phoned my young colleague to enquire whether the amounts of narcotics written on his prescriptions for this young woman and the alleged epileptic were indeed correct. My young colleague then noted that five pages had been removed from the back of his prescription pad. The oral contraceptive script of course already had his signature on it, and this had been forged onto the stolen prescription pages.

In country practice I had acquired the skills for tonsillectomy, a much over-performed operation in past years. A colleague from another country practice referred to me a 20-year-old woman for tonsillectomy. I thought that the tonsils were normal, but both he and the patient insisted they should be removed because of a recent shocking attack of tonsillitis. I obliged.

A few months later he rang saying he had a 23-year-old woman with another terrible bout of tonsillitis. This seemed most unusual and so I requested to see the patient the following day. Indeed she did have severe tonsillitis, but she also had petechiae on the soft palate widespread lymphadenopathy, splenomegaly and a positive Paul-Bunnell test.

I knew these things because I had been ‘caught out’ giving penicillin and ampicillin to patients for acute tonsillitis (streptococcal I thought!) only to have severe maculopapular rashes develop.

One evening a young lady, aged 18, presented to the emergency room of our hospital complaining of an offensive vaginal discharge. Offensive was an understatement! Further questioning established that it was possibly a retained vaginal tampon and sex had impacted it further.

I could readily see the tampon and removed it with sponge-holding forceps. The odour was overbearing and I staggered with weak knees to the toilet to dispose of the putrid object. An embarrassing stench (especially for the patient) pervaded that area of the hospital. I then mentally devised a scheme to make the procedure more aesthetic for all concerned.

The patient contacted me two days later to say that the problem persisted. I examined her again and there was another tampon and the same mousy discharge. I felt most embarrassed about being ‘overcome’ by the previous consultation and not checking that the vagina was ‘all clear’. This time I brought a plastic bucket of water to the introitus and plunged the tampon (still attached to the forceps) into the bucket. After checking that the vagina was empty I sped to the toilet, tipped the water and the tampon into the slush bowl and flushed it. Virtually no smell this time.

One of the liabilities for general practitioners in the day-to-day practice of their art is a direct consequence of one of the greatest assets of general practice—continuing care. When we see the same patient year in and year out—perhaps even 10 or 12 times a year—subtle changes in the patient are not noticed and are often camouflaged by a host of previously diagnosed neurotic symptoms. We are all aware that one day we will miss something important that the outsider—the consultant, the locum, the casualty intern or even the student—will detect instantly. We hope that this will not occur too often and pray that the outcome of our delayed diagnosis will not be sinister. This case illustrates such an occurrence.

Miss Davies, a 68-year-old spinster, had attended our clinic for 25 years and had been seeing me for almost six of those years. She had a history of cholelithiasis and reflux oesophagitis, and about two years ago had complained of neck pain and headaches. I had X-rayed her neck and found the usual spondyloarthritic changes to be expected in a lady of this age. The neural foramina were encroached on by osteophytes at C2 to 3, C3 to 4 and C6 to 7.

For the next two years I confidently and graciously explained away her neck pain and headache in terms of these changes. Then a final-year medical student was attached to our practice for two weeks and I asked her to interview Miss Davies, warning the student that she probably would hear a barrage of complaints about neck pain and headache. I allowed the student 10 minutes and then walked into the room and said somewhat sardonically, ‘Well, what did you discover?’

‘Don’t you think her head looks a little large?’ she replied. ‘Do you think she might have Paget’s disease?’

‘Oh no,’ I retorted, ‘Miss Davies has always looked like this’.

At this stage the patient interjected, ‘You know, Doctor, I’ve always been worried about getting Paget’s disease: my father died of it’.

‘Well, Miss Davies,’ I replied, ‘Paget’s disease, to the best of my knowledge, is not hereditary but to reassure you I’ll order a skull X-ray.’ The result of the X-ray: florid Paget’s disease.

Bernard is a keen sportsman who unfortunately suffered with severe pain around his right ankle for six long years until the elusive diagnosis was made and an instant cure provided. He was 34 years old when he first presented with the pain, which developed insidiously.

He consulted a rheumatologist who said that he had post-traumatic arthritis and that an X-ray that reported ‘some spurring on the dorsal surface of the neck and body of the right talus’ was of little significance (Figure 7.2).

Bernard first consulted me about 12 months after his problem started, when the pain became very severe, causing him sleepless nights unless he took non-steroidal anti-inflammatory drugs (NSAIDs). He described the pain as feeling ‘as though there was a nerve on edge’ but said the aspirin was very effective for pain relief. On examination of his right ankle there was acute localised tenderness on the anteromedial aspect of his ankle with some diffuse area of soft tissue swelling. The ankle joint was stable, and all movements and gait were normal. I referred him to an orthopaedic surgeon who was an expert on ankle disorders.

Surgery

The surgeon found a large area of discoloured irregular looking synovitis with bone erosions on both the talus and the anterior tibia. He said the diagnosis was uncertain and performed localised synovectomy, which was reported as ‘non-specific chronic synovitis’.

Post-surgical progress

Bernard’s pain continued relentlessly. The surgeon felt Bernard should be fine, but further visits to his rheumatologist did not help. The latter performed several tests including full blood examination (FBE), ESR, rheumatoid arthritis factor, uric acid, tissue typing and plain X-rays, all of which were reported as normal. Bernard was told that he had ‘a low-grade inflammatory joint disease, most likely of rheumatoid variation’ and that he would have to learn to live with it with the help of the effective NSAIDs. However, he battled on bravely even with the label of ‘neurotic’, which he himself was beginning to believe. Acupuncture and various other remedies were ineffective.

Five years later

When I met Bernard socially five years later, I was distressed to discover that in addition to his painful ankle he had a severe duodenal ulcer that was responsible for melaenas. He was now on ranitidine (Zantac) and naproxen (Naprosyn). He said that the ankle pain was worse than ever, especially at night. It was intense first thing in the morning when he put his foot to the floor. He then hobbled around for 15 minutes, but it did not bother him much during the day when he was occupied and busy.

‘Light switch’ and the solution

Something suddenly clicked in the sluggish grey matter. Could it be? I rang another orthopaedic surgeon and, yes, he thought an osteoid osteoma was a definite possibility. We organised a bone scan that showed a hot spot in the neck of the talus ‘suggestive of an osteoid osteoma’.

At surgery bone chiselling revealed the seemingly innocent little tumour that caused so much pain—the osteoma with its cherry red soft core about 8 mm in diameter. It was removed and the defect packed with bone wax.

Bernard has lived and slept happily ever after. Well almost! The epigastric pain of his old NSAID-induced peptic ulcer still reminds him of six years of relative hell!

Sheryl was a cheerful and apparently healthy 31-year-old nurse who had recently assumed nursing duties at our hospital, having worked in various centres while travelling around Australia over the past 12 years.

She soon presented with severe lower abdominal pain. I noted that her behaviour was somewhat bizarre. She was whimpering, agitated and writhing with severe colicky pain and vomiting. Examination revealed multiple scars on her distended abdomen, mild generalised tenderness and increased bowel sounds. The rectum was empty. She produced a letter outlining that she had suffered multiple bouts of severe abdominal pain, which had resulted in a total of 17 surgical procedures including an appendicectomy, a cholecystectomy, Billroth II gastrectomy, two ovarian cystectomies, hysterectomy, splenectomy, division of adhesions for bowel obstruction and several exploratory laparotomies. She was ‘allergic’ to pentazocine, morphine, barbiturates and codeine; pethidine was ‘the only effective treatment for the attack’.

DIAGNOSIS

My immediate diagnosis was pethidine addiction, although Munchhausen’s syndrome or bowel obstruction secondary to adhesions were possibilities. Management in hospital included an intravenous drip, nasogastric suction and chlorpromazine 25 mg by intramuscular injection. A plain X-ray of her abdomen showed no abnormalities. Several hours later when she felt comfortable a nurse reported that a urine specimen left on the bench was coloured red but negative for blood. The penny dropped!

The afternoon consultation was interrupted by a phone call from a local farmer describing a motor vehicle accident near his farmhouse. The driver had been injured when his car left the road and crashed into a tree.

At the scene of the accident a blood-spattered middle-aged man was stumbling around, apparently intoxicated but not smelling of alcohol. There were several lacerations on his scalp and face but otherwise he seemed free from injury. His somewhat irrational behaviour made it difficult to obtain a history.

The ambulance arrived and we decided to send him to the nearest base hospital, about 80 km away. I phoned the admitting officer in advance to tell him that ‘George’ (aged about 40), who was unknown to us, had sustained head injuries. By the time the ambulance reached the hospital the patient was comatose and unresponsive to verbal commands.

PROVISIONAL DIAGNOSIS

George was assessed by a surgeon who diagnosed an extradural haematoma and organised its urgent decompression.

Tension mounted as the unconscious patient was rushed to theatre, his wounds cleaned and his head shaved (a gleaming dome awaiting the surgical assault). The anaesthetist inserted an intravenous line while, in the wings of the operating theatre, the impatient and anxious surgeon waited to snatch yet another patient from the jaws of death. Then, as the surgical drama was about to unfold, the drapes began to stir and the patient roused from his afternoon ‘slumber’. Sitting upright on the operating table, he gazed around in bewilderment, and then began to deliver an emotional verbal assault punctuated by the ‘great Australian adjective’.

The bemused surgeon, known for his ability to have the ‘last word’, turned to the theatre sister with ‘Is there an item number for a head shave?’

REVISED DIAGNOSIS

The patient was an insulin-dependent diabetic; that afternoon he had been hypoglycaemic. It took only 100 mL of the 5 per cent intravenous dextrose routinely administered by the anaesthetist to correct the dangerously low blood sugar level.

Greta was a 49-year-old nurse who presented as a bright, bouncy, obese woman with a characteristic thick German accent. She often consulted me for various musculoskeletal problems, especially low back pain.

Over a period of four months, however, she presented with several problems mainly musculoskeletal and psychogenic in nature. Apart from constant backache, she complained of rheumatic aches and pains, especially around her shoulders and hips, with associated tingling feelings in her hands and feet. In particular she complained of feelings of anxiety and depression manifest as insomnia, irritability, tension-type headache, excessive crying, fatigue, feelings of hopelessness and loss of libido. Other significant complaints included weight gain, a creepy-crawly feeling over the skin, dryness of skin and hair, intolerance to alcohol, burning and itching around the urethral opening with a tendency to frequency, and flushing around the head and neck. She stated that her periods were still present but getting lighter. I was most concerned with her comment that she felt ‘life wasn’t worth living’. Apart from dryness of the skin and hair, obesity and obvious depression, physical examination was normal.

Investigations

Investigations included haemoglobin and film, ESR, thyroid function tests, random blood glucose and X-ray of the lumbosacral spine. All investigations were normal.

MANAGEMENT AND OUTCOME

Because of my concerns about her depression and possible suicide tendencies I commenced her on the antidepressant doxepin and recommended vitamin supplements. I counselled her about lifestyle and diet, especially for her problem of obesity.

On review she claimed to feel considerably worse on her antidepressants and had ceased to take them. She then produced several German health magazines and pointed out that her problem could be explained by a lack of hormones. She had diagnosed ‘oestrogen deficiency’ from reading the literature. ‘What do you think about giving me hormones?’

It became obvious that she was absolutely correct and that I had made a therapeutic blunder by not following the basic principles of correcting biochemical imbalance. I therefore prescribed Premarin 0.625 mg daily and Provera 10 mg for the first 10 days of the month.

Within three months she happily announced that she ‘felt like a new woman’. She said, ‘It’s a miracle—my aches and pains have gone, and my skin feels healthy again. I don’t feel tense or depressed. Isn’t it wonderful?’