Chapter 3: Masquerades and pitfalls

CASE 1

A 32-year-old housewife presented with 12 months of fluctuating symptoms of polyarthritis of the proximal (PIP) and distal interphalangeal joints (DIP) of the hand. Other symptoms included malaise, fever, mouth ulceration and Raynaud’s phenomenon. The only abnormal findings were evidence of Raynaud’s phenomenon in fingers, palmar erythema and mild fever but no deformity of the joints of the hand.

CASE 2

A 56-year-old farmer presented with 3 months of painful, swollen hands, wrists, feet and knees. Associated symptoms included severe fatigue, morning stiffness, intermittent grittiness of the eyes and mouth dryness. On examination he had synovial thickening and tenderness in the metacarpophalangeal and PIP joints and knees. He also had a dry mouth and conjunctivitis of the left eye.

CASE 3

A 17-year-old female student presented with 10 weeks of pain in her hands, wrists, knees, ankles, feet and shoulders. She also had swelling of the ankles and morning stiffness. She had been taking minocycline for acne for 12 months. Examination revealed tenderness of the left third PIP joint only.

CASE 4

A 30-year-old male salesman presented with 10 days of shortness of breath, cough, night sweats and chest pain. He described 12 months of mild, variable, intermittent pain of his hands, wrists and shoulders. On examination he had mild synovitis of the MCP and PIP joints of both hands and bilateral pleural effusions.

Tom was a popular medical colleague who was the envy of many because of his debonair bronze surfie looks and immaculate presentation. In fact he was so suave and attractive to the ladies that we called him ‘Hollywood Tom’. He reminded me of Charles Dickens’ Dr Jobling who was described thus:

Tom always looked a picture of health with his hallmark swarthy looks over the years. He did not smoke and drank alcohol socially only.

At a medical reunion we observed that the 60-year-old surgeon looked tired and thin. He confided that he was very tired and concerned about his weight loss. He did not have a general practitioner and had not sought a consultation but said that he was coming to see me for a check up. However, in a few days time we heard the sad news that his left leg suddenly gave way and he collapsed to the floor. He had a pathological fracture of the femur due to a metastatic deposit from a hepatoma which had developed in a cirrhotic liver caused by primary haemochromatosis. Tom died about five months later.

TWO CASES

‘Will you come and see Uncle Sam please—he’s having another of his mini strokes.’ Stroke number nine in fact! It was my very first week in country practice and I was bemused by the call. Sam P, a 72-year-old farmer, was quite well apart from his blackouts, and like doctors before me I could find absolutely nothing wrong with him. Apparently he would suddenly black out and recover after a few minutes. I asked him to arrange a consultation the following day.

Evelyn A, aged 68, was another local identity who kept complaining ad nauseam about vague feelings of fatigue, lack of energy and occasional light-headedness. After several visits to various doctors (including specialists) she would dismiss it as ‘getting old—but I hate not being my usual fit self’.

DIAGNOSES AND OUTCOMES

Both Sam and Evelyn had the problem of bradyarrhythmia—a paroxysmal cardiac abnormality that can be very difficult to detect. Sam’s complete heart block disorder manifesting as Stokes-Adams attacks were diagnosed by admitting him to hospital and attaching our brand new cardiac monitor (this was 1970).

Evelyn’s sick sinus syndrome was diagnosed using a 24-hour Holter ambulatory ECG. It was disturbing to realise that she had suffered with its manifestations for six years before the cause of her sluggishness and light-headedness was determined.

The two patients were given a new lease of life with the insertion of pacemakers. Sam was given one of the first pacemakers in our part of the country.

My relative Joy T, aged 65, initially ‘consulted’ me at a family gathering. She described a problem of extreme fatigue: ‘I cannot get out of my own way—I feel so weak’. The fatigue, which had been getting progressively worse over the past four months or so, was associated with weakness, anorexia and ‘depression’. Furthermore, she complained of dyspnoea and chest tightness on moderate exertion, with occasional palpitations.

She had a history of a myocardial infarction three years before with subsequent congestive cardiac failure. She also had a 12-year history of late-onset bronchial asthma requiring maintenance oral prednisolone of 5 to 10 mg. Her medication was digoxin 0.125 mg, amiloride 5 mg—hydrochlorothiazide 50 mg (Moduretic), beclomethasone and salbutamol nebulisers, and prednisolone 10 mg daily.

She certainly looked unwell and so I advised her to return to her general practitioner as soon as possible for review. After examining her, he mentioned that her ‘chest was in poor shape and that the heart was faster than normal’.

Joy’s general practitioner referred her to her cardiologist who performed a battery of tests including an electrocardiogram, chest X-ray and serum electrolytes. He informed her that unfortunately she had deteriorating cardiac failure and that her potassium was too low. He prescribed potassium supplements and increased her digoxin to 0.25 mg.

Four weeks later Joy contacted me to say that she felt no better, was very depressed, had lost weight and wished that she could die.

Diagnostic probabilities

When contemplating her problem on my way to see her, I thought that she could have digitalis toxicity and perhaps diabetes mellitus (especially being on a thiazide diuretic and prednisolone) or could have a psychological problem such as depression. However, when I saw her the striking feature was her pallor. ‘Everyone says I’m grey but the specialist said it was due to my heart’, she said. I decided to order a full blood examination, serum digoxin and random blood sugar.

I was not surprised when the results revealed a haemoglobin of 67 g /L, due to iron deficiency. She had no history of bleeding but a faecal occult blood test was positive.

DIAGNOSIS AND OUTCOME

Joy was admitted to hospital for blood transfusion and endoscopy. Gastroscopy revealed severe oesophagitis at its lower end. The conclusion was that her iron deficiency anaemia resulted from oesophagitis, possibly caused by corticosteroid therapy.

Mrs EP, a 55-year-old divorced schoolteacher, first presented to me complaining of a two-week history of proximal muscle pain and weakness in her shoulders and, to a lesser extent, her pelvic muscles. She was tired and lethargic.

My eyes lit up as I confidently made a provisional diagnosis of polymyalgia rheumatica—classic textbook material.

Initial management

The ESR of 51 supported my provisional diagnosis and so I commenced her on 30 mg prednisolone. She returned earlier than the arranged weekly review complaining of worsening symptoms. Because she lived alone, with little support, I decided to admit her under my care to the local hospital. She eagerly agreed to this decision. The plan in hospital was to continue with the steroids, provide an opportunity for rest and await the expected improvement.

A negative response

However, the plan changed as she continued to complain of muscle pain and tenderness despite continued corticosteroids. I became uneasy about the diagnosis of polymyalgia rheumatica. I arranged investigations to exclude other inflammatory and connective tissue disorders and sought an opinion from a rheumatologist. On his advice, in the presence of a rising ESR (now 79), the provisional diagnosis remained unchanged. However, the dose of steroid was increased to 50 mg daily.

General confusion

After a few days in hospital, Mrs EP became confused and complained of severe lower abdominal pains associated with nausea and frequent non-watery bowel motions. She also complained of electrical feelings through her body and other hallucinations. Examination revealed marked lower abdominal tenderness but no signs of peritonitis. Concerned about the possibility of an acute bowel perforation (secondary to the high steroid dosage) I asked a surgeon to assess her (despite normal plain abdominal X-rays). His diagnosis of acute diverticulitis (aggravated by the steroids) was confirmed by barium enema. She settled well on intravenous antibiotics and analgesia. At the same time serum electrolytes, a full blood count and liver function tests were performed. To my surprise her liver function tests were abnormal, with marked elevation of gamma glutamyl transferase and alkaline phosphatase, consistent with alcoholic liver disease. This was a salutary lesson to me, as up to that point I had never inquired specifically about her alcohol intake, nor had it entered my mind to do so in the clinical context.

In retrospect, Mrs EP’s odd behaviour soon after admission was probably an acute brain syndrome (due to alcohol withdrawal) rather than related to her medications or underlying illness.

Management and counselling

I felt it was important to confront her with these results and ascertain an exact indication of her level of alcohol consumption. After a brief period of denial, she admitted to consuming increasingly larger quantities of alcohol—in the order of one flagon of sherry daily.

For the next few days the focus of my daily visits changed from concentrating on the biological disease to helping her cope with her drinking problem. With the strengthening of the doctor–patient relationship her ability to discuss personal problems increased. It became evident that she had a full complement of risk factors, which had been previously overlooked.

A consultant (with a special interest in alcohol abuse) visited her in hospital and she developed a good working relationship with him. Various members of the hospital’s nursing staff also provided valuable support over the first few days. Mrs EP found solace in religion and received a constant stream of visitors from her church community, who were able to provide the reassurance and confidence that she needed.

After nearly three weeks in hospital, she was discharged and a good network of support arranged. After six weeks her liver function tests had returned to normal and she states that she has not had a drink since. Soon she returned to teaching and appears to be coping very well.

SAGA 1: HOT FLUSHES

A 29-year-old married motor mechanic consulted me for the first time, complaining of episodes of facial flushing associated with ‘blotchiness’ of the skin of his trunk and difficulty in breathing. Sometimes he would feel very ill and eventually vomit. He said the symptoms occurred only when he drank beer, but not every time. When he drank beer he would usually smoke cigarettes. He said he was taking no medication and had no history of atopic disease. Examination was unremarkable. I told him I thought he had an allergy and considered a possible carcinoid tumour. We agreed he would take further note of his episodes and report to me.

I next saw him three months later for a ringworm infection. He said the flushing episodes had resolved spontaneously, and so we let the matter rest.

About two years later he was ‘retrenched’ from his job while on holiday, and his wife came to see me. She said he was drinking heavily. It emerged that he had been abusing alcohol for many years. As she described the effects of his drinking on their marriage and young family, she confided that in her desperation to help him she had on several occasions ‘spiked’ his coffee with disulfiram (Antabuse), obtained when he had once attended an alcohol rehabilitation program. She was aware of the link with his flushing symptoms and was surprised that I had not realised what was causing them.

This story is a reminder that alcoholism can present in many ways: in this case, the surreptitious administration of medication by a worried family member.

SAGA 2: EXCHANGING MILK FOR BEER

George, a 49-year-old dairy farmer and former army officer, presented with gouty arthritis and dyspepsia. He had a history of hypertension, which had deteriorated in recent years.

His plethoric bloated facies and continued complaints of anxiety and insomnia made me question him carefully about his alcohol intake. ‘I have only a glass or two a day, Doc. It’s not a big deal: ask the wife and the boys at the pub and the RSL club’, was George’s emphatic reply.

With time and a steady rise in his blood pressure, plethora and anxiety, and a continuing decline in his general health and libido, I strongly suspected a considerable intake of alcohol. I checked his story with his wife and the ‘boys’ at the local hotel. They confirmed his relatively sober habits.

Eventually George developed a cardiac arrhythmia and had to be admitted to hospital. His convalescence provided his bemused visitors with a somewhat convincing swatting of spiders on his bed with his slippers and description of the non-existent circus parading through the town. George and his family continued to deny the alcohol problem: ‘Get off the bandwagon for God’s sake—I have only the odd one’, he said.

One day, while treating the milk-tanker driver, I casually asked him how many bottles of beer he delivered to George. After an uncomfortable pause, the expected revelation was made: ‘A dozen large bottles every other morning’.

The outcome was eventually positive. With the help of Alcoholics Anonymous, George managed to control his addiction and now enjoys better health but I remain concerned.

Why do we often refer to herpes zoster (shingles) as one of the pitfalls or causes of a ‘red face’ for the general practitioner?

The reason is that it can present as pain well before the onset of the characteristic vesicular rash in the dermatome or dermatomes. It is common for two or more contiguous dermatomes to be involved especially in the thoracic dermatomes. The patient may be given an inappropriate diagnosis (often guesswork) or treatment prior to the diagnosis.

There is a prodromal or window period of about 2 to 3 weeks. Sometimes we have administered physical therapy to the spine for spinal dysfunction—quite an embarrassment! A particular diagnostic brain teaser is where only one or two maculopapular eruptions appear in the dermatome and which are separated by considerable space.

CASE 1

In the example shown a 38-year-old butcher presented with a painful lump on his back adjacent to the spine. He said that it felt like a boil but when his wife introduced a needle it drained only a small amount of blood and no purulent material. It was only when he was stripped of clothing and closely examined that the other two lesions were observed on the anterior chest wall. It was herpes zoster of dermatome T7.

CASE 2

A 55-year-old hairdresser presented with the pain of classic right-sided sciatica involving the L5 dermatome which was not alleviated by over-the-counter analgesics. While testing her reflexes I noticed two vesicular lesions on the outside of her leg at the level of the knee. She had herpes zoster.

It was during consulting hours on the Australia Day holiday that the receptionist for our group practice contacted me saying, ‘I have a gentleman who doesn’t want to see you but insists on a prescription for Ventolin. Could you oblige?’

The practice rule is not to prescribe without seeing the patient. When I left my consulting room I noticed a very formidable, impatient character pacing around looking rather like a Hereford bull waiting for springtime—massive, plethoric, humourless and with a RAAF-like moustache. He was an arrogant 56-year-old business executive.

His confrontation was incisive and threatening: ‘Bloggs of Bentleigh, Doc. I just want a script of Ventolin for my asthma—haven’t got time to wait around’. Despite my feelings of annoyance I thought it expedient to follow the soft option and I quickly scribbled a script for the simple anti-asthmatic drug.

Three months later on Easter Saturday, the receptionist informed me that a man was at her desk wanting a repeat of his ‘blood pressure pills’. It was Bloggs, who reluctantly agreed to my insistence that he should wait to be seen. In swaggered Bloggs—arrogant, fidgety, very plethoric, obese, the sound of wheezing punctuating his laboured alcohol-saturated breath, uncomfortable about his subordinate role.

‘I’ve had this asthma on and off for two years ever since you fellows changed my blood pressure tablets.’ As I perused his history the answer became painfully obvious.

DIAGNOSIS

Two years previously the patient’s antihypertensive therapy was altered when metoprolol was substituted for methyldopa. At the same time the attending doctor stressed the importance of reducing weight, smoking and alcohol intake. The change to a beta blocker precipitated bronchial asthma, which had been quiescent since his adolescence.

Many years ago Claude, a 52-year-old farmer, presented with vague abdominal pain. On examination he had an abdominal mass that was found to be lymphosarcoma. Extensive surgery helped, and he was referred to an oncologist at a major city hospital for continuing management of his nasty tumour.

After the first intravenous injection of the cytotoxic agent cyclophosphamide, he became very sick (pallor, vomiting and faint) on the long drive back to the country. I was called to his home immediately and found that he was pale and sweating, and hypotensive. I spent an hour or so with him, during which time he gradually improved with his blood pressure returning to acceptable limits. I considered that this was a severe toxic reaction to the cytotoxic drug.

I wrote a letter to the oncologist requesting that consideration be given to changing or modifying the drug for his next treatment a couple of weeks later. Claude felt quite well at this visit. When the letter was read the rather glib reaction was ‘funny business—lot of stress with this business you know—car sickness is a problem too’. So the injection was repeated and Claude was driven back home. I was attending a delivery at our small hospital when the car pulled into the emergency bay. Claude was dead. He had had the same symptoms on the way home and had ‘collapsed’ about 10 km from home.

CASE 1

Marge T, aged 52, presented with an extraordinary story of modern medical mismanagement. While carrying heavy suitcases in Hong Kong she developed anterior chest pain. She was taken to an emergency department where, despite a normal ECG, she was told she had heart trouble and had to be careful.

Upon returning to Melbourne and while under the care of her son-in-law, who was a specialist, she developed episodes of central chest pain with, at times, mid-thoracic back pain. She felt tired and languid. A stress ECG was normal. She was admitted to a teaching hospital for further investigation. Unfortunately, an ultrasound examination was reported to be abnormal (? chronic relapsing pancreatitis). The incompatible clinical history was ignored as she went from investigation to investigation over a period of nine months. The eventual diagnosis was chest pain of unknown cause with anxiety.

DIAGNOSIS AND OUTCOME

The anxious and devastated Marge, as a result, first consulted me with classic depression. The history was interesting—the pain invariably followed a lifting or laborious activity such as vacuuming and bed-making. The associated back pain tended to get ignored as the focus was on the retrosternal pain. Examination revealed tenderness at the T5 and T6 levels of her thoracic spine while a plain X-ray showed mild degenerative changes.

She had dysfunction of her mid-thoracic spine with referred pain. After three treatments by spinal mobilisation and manipulation, her pain completely subsided as did her ‘stress-related problem’, anxiety and depression (although it took some months).

CASE 2

Elana W, aged 32, presented as a new patient with epigastric pain brought on by physical activity including lifting her children. A careful history determined associated back pain ‘just around my bra strap’. The problematic T7 area of her thoracic spine was appropriately treated.

Elana came in with one of her children some weeks later and said, ‘You know, Doctor, that stomach pain I’ve had for three years has gone. To think that it was thought to be an ulcer and then a hiatus hernia. I’ve had two barium meals and a tube passed down but they found nothing.’

CASE 3

Joan G, aged 41, requested a second opinion about recurrent pains under her right costal margin for 12 months or so. Cholecystectomy did not help at all, but correction of her thoracic spinal problem at T7–T8 completely alleviated the pain.

CASE 4

The writer has a personal testimony worth recording. Poliomyelitis affected the back at 8 years of age and then from age 12 to 24 with persistent thoracic back pain that would radiate antero-laterally just below the nipple line, either right or left side. ‘You have to learn to live with it John—it will probably get worse as you get older’, came the reassuring prognostication from my attending neurologist.

Other more adventurous doctors proffered diagnoses such as post-polio neuralgia, da Costa’s syndrome and Tietze’s syndrome. I noted during medical school that if patients were unfortunate enough to get the pain on the left side of the chest it was called ‘cardiac neurosis’.

However, while attending a football club physiotherapist for an ankle injury, he noted my thoracic deformity and asked if it gave me pain. ‘I can fix that.’ ‘No, you can’t.’ ‘Yes, I can—let me try.’ Thumbs and hands deftly worked on the T4–T6 levels—impressive sound effects with cracking and clicking. To the profound relief and gratitude of this impressionable patient, the 13 years of pain was relieved. Yes, it returns occasionally but is likewise fixed with physical therapy.

Molly W, aged 78, came in with her shopping list of symptoms, one of the ‘heartsinks’ of a frantically busy practice. With slow, monotonous deliberation the problems were reeled off. ‘I feel sick, Doctor—you know nauseous, not myself, no energy, off my food, constipated, headachy, sore in the back, sore tummy, no get-up-and-go, not sleeping well, everything is an effort, I get thirsty and I tire out easily.’

‘Typical general practice problem,’ I mused, ‘undifferentiated illness—epidemic proportions this week’. Could she be hypothyroid? Polymyalgia rheumatica? Anaemia? No, she must be depressed with a history like that.

DIAGNOSIS AND OUTCOME

I ordered haemoglobin, blood film, ESR, random blood sugar and thyroid function tests. All these tests were normal. Upon review she said that she felt much the same, but the anorexia and nausea had increased and she felt hot and clammy. I was convinced that she was depressed, but I remembered to attend to a routine that I overlooked on the first visit—an office test of the urine. To my surprise (and relief) it showed positive to protein, blood and nitrite. Microscopy of the urine showed copious pus cells and bacteria. All her symptoms had virtually abated two days after commencing antibiotics.

ANNIE

Annie, a 23-year-old secretary, presented with a three-day history of diarrhoea with blood and mucus, abdominal pain and general malaise. She had had a diarrhoeal illness two months before this presentation, which settled spontaneously with normal bowel action up until the recent presentation. Her history was unremarkable apart from appendicectomy. She was on the oral contraceptive pill. In particular, there was no other bowel disturbance or family history of bowel disease. A general examination showed a relatively fit person with a soft abdomen and a rectal examination revealed soft stool. Sigmoidoscopy to 10 cm showed an inflamed, ulcerated rectum with some contact bleeding.

In view of the severity of proctitis and concern of ulcerative colitis, urgent gastroenterological referral was organised. The consultant’s diagnosis was ulcerative colitis. Biopsies were taken and sulfasalazine commenced. The biopsies were consistent with ulcerative colitis.

Nausea and persistent malaise on sulfasalazine prompted a change to mesalazine. Fortunately stool cultures had been obtained by the gastroenterologist and Campylobacter jejuni was cultured. Mesalazine was ceased and erythromycin prescribed. Subsequently all symptoms settled, much to the patient’s joy and her doctor’s relief.

KAY

Kay U, a 29-year-old mother of two young children, presented 10 days after Annie. She had a longstanding history of ulcerative colitis. She had experienced numerous (two to three per year) severe flare-ups requiring high dose oral and local corticosteroids with ongoing maintenance with sulfasalazine. She presented with what appeared to be a further exacerbation with abdominal pain, diarrhoea with blood and mucus. She commenced oral prednisolone (30 mg per day) and rectal hydrocortisone. However, her symptoms did not improve and contact with her gastroenterologist prompted further increase of the oral corticosteroid.

Persistent failure of her symptoms to improve prompted the gastroenterologist to request admission to our local country hospital for high doses of intravenous hydrocortisone and bedrest with nil orally. Fortunately, in view of our recent experience with Annie and despite Kay’s well-known ulcerative colitis, he advised us to organise stool cultures.

After several days of high-dose steroid, the patient had some significant improvement in stool function and was feeling significantly better and desperately hungry. Stool cultures paradoxically were positive for Campylobacter jejuni and erythromycin was prescribed and steroids reduced. Fortunately again, stool function returned to normal.