Материал: 100_Cases_in_Clinical_Medicine

CASE 79: CONFUSION

History

A 79-year-old woman is brought to hospital by her daughter because of increasing confusion. This has developed over the last 3 weeks and prior to this her daughter says that she had normal cognitive function. She also complains of loss of her appetite, headache and muscle cramps. She had hypertension diagnosed 5 years ago and was on treatment with atenolol but this was stopped 2 months ago because she complained of cold hands and feet. Her medication was changed to bendroflumethiazide 2.5 mg once a day and she has had no problems with these tablets. She lives on her own with her daughter nearby. She neither drinks alcohol nor smokes. She is on no other medication although she takes vitamins that she buys from the chemist.

Examination

Her skin turgor is normal. Her pulse is 80/min regular, blood pressure 146/90 mmHg, jugular venous pressure normal, heart sounds normal with no peripheral oedema. Respiratory and abdominal systems are normal. Her abbreviated mental test score is 6/10 with disorientation in time and place. There is no focal neurology. Funduscopy shows silver-wiring and arteriovenous nipping but no papilloedema.

INVESTIGATIONS

Questions

•What is the likely cause of this patient’s confusion?

•How would you correct this problem?

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ANSWER 79

This woman’s confusion is due to hyponatraemia. There are many causes of confusion in the elderly but the very low sodium level of 113 mmol/L in this case is an adequate explanation. Her serum is profoundly hypo-osmolar. In her case, osmolality can be calculated from the following equation:

2 % ([Na'] ' [K']) ' [urea] ' [glucose] ) 241 mosmol/kg (normal range: 278–305 mosmol/kg).

Hyponatraemia may be asymptomatic, but when it falls rapidly or reaches very low levels (below 120 mosmol/kg) it can cause confusion, anorexia, cramps, fits and coma. Hyponatraemia is associated with hypovolaemia when there is excess loss of fluid and sodium (sweating, burns, diarrhoea and vomiting), or when there is renal loss of sodium and water (diuretic use, Addison’s disease).

Hyponatraemia with hypervolaemia occurs when there is excess retention of water. Normally, the dilutional fall in plasma osmolality suppresses arginine vasopressin (AVP, antidiuretic hormone) secretion which allows excretion of excess water. In congestive cardiac failure and cirrhosis with ascites, baroreceptors register reduced perfusion causing AVP secretion, but in most other cases of hyponatraemia there is an inability to suppress AVP secretion normally. In rare cases of primary polydipsia, the huge water intake may overwhelm this mechanism, and in severe renal failure the kidneys cannot excrete a water load.

The syndrome of inappropriate anti-diuretic hormone secretion (SIADH) occurs in relation to malignancy, neurological disorders or pneumonia. Circulating volume is usually normal. Normovolaemia with hyponatraemia also occurs after administration of too much intravenous hypotonic fluid and in hypothyroidism.

The low plasma sodium, potassium and urea in this patient are consistent with water excess. Measurement of urinary sodium and osmolality is useful. In primary polydipsia the urine can be maximally diluted to !100 mosmol/kg, whereas in states with excess AVP the urine osmolality is usually #320 mosmol/kg while plasma osmolality is low. Urinary sodium is usually !25 mmol/L in hypovolaemic states, but #40 mmol/L in SIADH where patients are normovolaemic and the rate of sodium excretion depends on dietary intake and taking of diuretics. Diuretic-induced hyponatraemia tends to occur within a few weeks of starting treatment, and occurs mainly in elderly women often concurrently on non-steroidal antiinflammatory drugs (NSAIDs) which inhibit water excretion. The clinical and biochemical picture in this woman is consistent with diuretic-induced hyponatraemia.

KEY POINTS

•Low plasma osmolality with high urinary osmolality suggests excess ADH production.

•Volume depletion with urinary sodium #20 mmol/L suggests water and sodium loss through the kidneys (renal failure, diuretic use, Addison’s disease).

•Volume depletion and low urinary sodium (!20 mmol/L) suggests volume and sodium loss extrarenally, e.g. vomiting, diarrhoea, sweating.

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CASE 80: PAIN IN THE LEG

History

A 38-year-old woman presents to the emergency department with a painful left calf. She had woken that morning to notice that her calf was swollen and found it painful to put her foot to the ground. There was no history of recent air travel or long-distance car journeys. She is otherwise well, is not breathless and has no chest pain. She has had no previous medical illnesses other than some cartilage problems in the knees. In her obstetric history she has had two first-trimester miscarriages and has not had any successful pregnancies. There is no family history of note. The patient is married. She is a teacher of physical education and exercises regularly. She neither smokes tobacco nor drinks alcohol. The oral contraceptive is the only medication that she takes.

Examination

She is a little overweight. Her left leg is clearly swollen, with a 4 cm difference in circumference around the left calf measured 10 cm below the tibial tuberosity. There is tenderness on palpation of the calf. The left calf is slightly warmer than the right. There is a small effusion in the right knee, which is not hot or painful. There is some pitting oedema in the left ankle and there are superficial veins evident in the left leg. Physical examination is otherwise normal.

INVESTIGATIONS

Activated partial thromboplastin time: prolonged

Questions

•What is the cause of the swollen leg?

•How would you investigate and manage this patient?

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ANSWER 80

The most likely clinical diagnosis in this patient is a left deep vein thrombosis (DVT). The main differential diagnoses of an acutely swollen leg are a ruptured Baker’s cyst, trauma and acute cellulitis. Other causes of chronically swollen legs are obesity, lymphoedema, congestive cardiac failure and previous DVTs (postphlebitic). The knee cartilage problems raise the possibility of ruptured Baker’s cyst, and the active lifestyle is compatible with muscle trauma such as a ruptured plantaris but there is no story of an acute onset.

The raised D-dimers are not helpful since there are many causes. D-dimers are helpful when negative in making the diagnosis of DVT much less likely. The history of miscarriage and the raised activated partial thrombopastin time suggest the presence of antiphospholipid syndrome (lupus anticoagulant) which should be investigated together with serological tests for systemic lupus erythematosus.

!Scoring system for DVT diagnosis

In assessing the clinical likelihood of a deep vein thrombosis scoring systems are available:

!Major risk factors for DVTs

•Dehydration, prolonged inactivity, bedrest, post-surgical, obesity.

•Malignancy: cancers of the lung, pancreas, breast, prostate and gut are particularly associated. Pelvic malignancy causing compression can directly lead to venous thrombosis.

•Oral contraceptives: oestrogens increase the risk.

•Genetic causes: protein C/S deficiency, antithrombin III deficiency, homocystinuria and factor V Leiden mutation.

•Behçet’s syndrome: a diagnostic triad of iritis, orogenital ulceration and DVTs.

•Antiphospholipid antibody syndrome.

When a patient presenting with a DVT is young, or where there is no obvious underlying cause or where there is a strong family history or a history of recurrent events, underlying risk factors should be investigated. This woman had oral contraceptive use and the presence of antiphospholipid antibodies as risk factors for her DVT. Antiphospholipid antibodies may be present as part of systemic lupus erythematosus (SLE) or may be an isolated

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finding, primary antiphospholipid antibody syndrome. Although the antibodies prolong the activated partial thromboplastin time (APTT) they predispose to thrombosis. Recurrent miscarriages, as in this patient, may be a feature. Patients may present with idiopathic recurrent DVT, arterial gangrene, livedo reticularis, cerebral infarcts, chorea and multiinfarct dementia.

Doppler ultrasound of her leg veins will confirm the diagnosis of DVT. A thrombophilia screen should be sent. Lupus serology should also be performed to define if the antiphospholipid antibodies are part of SLE in this patient.

This patient should be immediately anticoagulated either with intravenous heparin or subcutaneous low-molecular-weight heparin to prevent proximal propagation of the thrombus and pulmonary emboli. The patient should be started on warfarin. Patients with antiphospholipid antibodies require lifelong anticoagulation and consultation with a haematologist to prevent further thrombotic events.

KEY POINTS

•Young patients with venous thromboses should be investigated for underlying causes.

•Patients with antiphospholipid antibodies require lifelong anticoagulation.

•Clinical diagnosis of a deep vein thrombosis is insensitive and has poor specificity.

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