Confusion Flashcards
(33 cards)
Mrs Doolally is an 84-year-old woman who is referred by her general practitioner (GP) to her local hospi- tal. She attends with her daughter, who reports that her mother is usually forgetful. However, when she visited that day she found that her mother was much worse than when she last saw her 3 days previ- ously, as she was very ‘confused ’ and ‘not herself ’.
‘Confusion’ is a very vague term that can refer to various medical syndromes, e.g. dementia, psychosis, etc.
What syndromes can cause a patient to appear ‘confused’?
• Delirium: an acute impairment in cognitive ability together with impaired consciousness.
• Dementia: a chronic, progressive impairment in cognitive ability but with intact consciousness. Note that this is different from delirium and that you cannot diagnose dementia from a single mental status assessment.
• Mental impairment: a permanent impairment in cognitive ability.
• Psychosis: the patient may not be confused, but hallucinating or deluded due
to a deranged personality and loss of contact with reality.
• Receptive dysphasia: the patient may have difficulties comprehending your questions (e.g. due to damage to Wernicke’s area of the brain).
• Expressive dysphasia: the patient may be cognitively intact but have difficul- ties verbalizing an answer to your questions (e.g. due to damage to Broca’s area of the brain).
t is often difficult to take a good history from a confused patient. However, you should nevertheless try to get some basic information from her.
What questions should you ask of all confused patients?
Remember to start by checking the patient’s airway, breathing, and circulation (ABC) and whether they are in any pain that requires analgesia.
To work out what type of confusion this is, you should start by conducting a quick screen of confusion because if the patient does poorly in your screen, taking a conventional history may prove unhelpful. For this, you should ask all confused patients:
• Are they oriented to time, place, and person? Can they tell you why they are here? The Abbreviated Mental Test Score (AMTS) is a simple 10-question screening tool for assessing confusion where a score of less than 6/10 indi- cates cognitive impairment. An alternative is the 30-question Mini Mental State Exam (MMSE), where a score of less than 26/30 indicates cognitive
impairment.
• Can they follow a three-step command? This tests for receptive dysphasia.
• Can they name three common objects? This tests for expressive dysphasia.
• Other symptoms? Are they in pain? (even the most confused patient will complain of pain). You should also ask about breathlessness, cough, and uri- nary symptoms as a chest or urinary tract infection (UTI) is often the cause of confusion.
Describe the AMTS
Remember this address: 33 Dorchester Street
Orientation in time
What time is it (nearest hour)? What year are we in?
How old are you?
Orientation in space
What building are you in?
Orientation in person
Who am I? Who is that person (e.g. nurse)?
Long-term memory
What is your date of birth?
What year did the Second World War end (or alternative date, e.g. particular Olympic Games)? Who is the current Prime Minister?
Short-term memory
Please count backwards from 20 to 1. Can you remember the address I told you?
Score < 6 = dementia or delirium likely
If they are accompanied, what information should you try to ascertain from their companion?
If they have been accompanied by someone who knows them, try to ascertain:
• Their normal state. It may be that they are behaving no differently from how they normally behave, but that it has been mistaken for confusion (e.g. if they have dementia, psychosis, mental impairment, etc.).
2
22 Confusion
• The time course of their confusion. An acute onset argues against dementia
and in favour of delirium.
• Their drug history (including alcohol). Any number of drugs can cause con- fusion. Consider both the introduction and cessation of drugs.
Why is the history from the person they are accompanied by important
This information is particularly important in elderly patients who may have dementia and/or be taking a number of medications which may or may not have changed recently. Remember that a history of dementia does not exclude an acute confusional state. On the contrary, such patients are at a greater risk of developing confusion in addition to their dementia.
If the patient has scored poorly on your quick screen of confusion and they are unaccompanied, you should move on quickly to the examination as conversation with the patient is unlikely to be productive.
Mrs Doolally is drowsy and confused with an AMTS of 5/10. She is able to follow a simple three-step command and correctly name three common objects. She reports that she fell over but otherwise is not sure why she has been brought in. She reports no other symptoms. Her daughter reports that her mother does not drink any alcohol. She takes a thiazide diuretic for hypertension, and is currently taking lactulose for constipation and clotrimazole for thrush.
Before you move on to examine Mrs Doolally, you should start formulating an idea as to what might be the cause of her acute confusion (delirium).
What causes of delirium can you think of?
The list is long and you may find using a surgical sieve is helpful.
Which of the diagnoses in your list are most likely in Mrs Doolally?
There are a number of different mnemonics for remembering a surgical sieve. The one used below is ‘INVITED MD’. The diagnoses more likely in Mrs Doolally, given both what is most common and her age, are given in bold type.
Infectious (e.g. chest, urinary, encephalitis, brain abscess, sepsis)
Neoplastic (e.g. brain tumour)
Vascular (e.g. stroke, myocardial infarction causing hypoperfusion)
Immune (e.g. rare conditions such as neuropsychiatric lupus, Hashimoto’s encephalopathy)
Trauma (e.g. subdural haematoma, extradural haematoma)
Endocrine (e.g. hypothyroidism, hyperthyroidism, diabetic ketoacidosis)
Drugs (e.g. intoxication or withdrawal of alcohol, opiates, or psychiatric medications; or use of diuretics, digoxin, thyroid medication). Drug toxicity accounts for 30% of delirium
Metabolic (e.g. hypoxia, hypercapnia, hypoglycaemia, sodium or other electrolyte imbalances, thiamine, folate, or vitamin B12 deficiencies)
Degenerative conditions. These will be chronic and will not cause the delirium, but they will predispose patients to becoming delirious
† In elderly patients, don’t forget that they may be hypothermic
Prior to taking a full history you should have checked Mrs Doolally’s vital signs, to ensure that they are
stable. These also provide some diagnostic information.
What vital signs would you be most interested in and why?
The vital signs of particular interest are:
• Pulse and respiratory rate: a tachycardia or tachypnoea could occur second- ary to sepsis or haemorrhage.
• Blood pressure: hypoperfusion of the brain (due to systemic hypotension) decreases patient consciousness. Also consider the relationship between the pulse and blood pressure – is there hypertension and bradycardia? This is known as the Cushing response and is indicative of raised intracranial pressure.
• Oxygen saturation: hypoxia also affects consciousness and can be easily measured with a pulse oximeter.
• Temperature: fever may indicate an underlying infective process. Alternatively hypothermia also causes confusion and is not uncommon in the elderly.
• Blood glucose: hypoglycaemia or hyperglycaemia can depress conscious- ness. In patients with type 1 diabetes hyperglycaemia may be associated with ketoacidosis (which also affects the mental state). In type 2 diabetics, extreme hyperglycaemia may indicate a hyperosmolar non-ketotic (HONK) state. A BM (capillary glucose) is sufficient at this stage, although any abnormal result should be followed up with a venous blood sample.
Mrs Doolally’s pulse is 108 bpm, her respiratory rate is 20/min, and her blood pressure 90/60 mmHg. Her oxygen saturation is 96% on room air, her temperature is 37.6oC and her blood glucose is 5.6 mM.
Confused patients may be inattentive, drowsy, and/or uncooperative, making a full examination difficult. Given this and the most likely diagnoses in your differential:
What are the most important signs to look for?
Even with patients who are difficult to examine, you should be able to do the following:
• Consciousness: assess this using the Glasgow Coma Scale (GCS). This was developed before head imaging modalities (computed tomography (CT) and magnetic resonance imaging (MRI)) where widely available and is a good prognostic indicator. It also enables you to track progression.
• Septic focus: look for evidence of a septic focus such as:
− Chest: look for signs of infection on percussion (dull) and auscultation
(bronchial breathing, crackles).
− Urine:checkforsuprapubictenderness,andifthereisacatheterbagcheck
whether the urine is cloudy and send off a specimen for microscopy, culture,
and sensitivities (MC&S).
− Cellulitis: carefully inspect the skin. In diabetics pay particular attention
to the feet, checking between the toes, as these are particularly vulner- able. Also check for any venous or arterial lines that may be a focus for infection.
− Meningitis: check for neck stiffness and a purpuric rash suggestive of meningitis.
- Pupils: check these, looking for symmetry, size, and direct and consensual responses to light. You may find fixed dilated pupils (drug overdose, e.g. cocaine, tricyclic antidepressants; severe hypoxia; hypothermia; post-ictal), fixed pin- point pupils (opiate or barbiturate overdose), or asymmetrical pupils suggestive of coning secondary to raised intracranial pressure or a third nerve palsy.
- Focal neurological signs: look for signs of focal neurological pathology (e.g. suggesting stroke or a space-occupying lesion): dysphasia, visual field defects, nystagmus, tone and reflex symmetry, plantar responses, focal weakness (mov- ing all limbs if not cooperating), ataxia, and sensory or visual inattention.
- Needle track marks: suggests intravenous (IV) drug abuse.
- Cherry red lips: occurs in carbon monoxide poisoning …or lipstick.
- Asterixis (metabolic flap): suggests hypercapnia, hepatic encephalopathy, or uraemia as a cause.
• Breath for alcohol, fetor hepaticus (liver failure), uraemic fetor (renal failure),
fruity (ketones in ketoacidosis).
• Bitten tongue and/or posterior shoulder dislocation suggests a convulsive seizure.
Describe the GCS
Glasgow Coma Scale
Best motor response
Moves arms in normal manner 6 Localizes hands to painful stimulus (e.g. push finger into angle of jaw) 5 Withdraws from painful stimulus (e.g. press hard on finger nails) 4 Flexes all limbs in response to pain 3 Extends all limbs in response to pain 2 No movement in response to pain 1
Glasgow Coma Scale (Continued)
Best verbal response
Talks fluently 5 Talks, but not fluently 4 Says words but sentences make no sense 3 Makes noise in response to painful stimulus 2 Silent despite painful stimulus 1 Best eye response
Eyes are spontaneously open and blinking naturally 4 Opens eyes in response to verbal command 3 Opens eyes in response to painful stimulus 2 Does not open eyes despite painful stimulus 1
GCS ≤8/15 = Patient cannot maintain own airway and will need a definitive airway i.e. intubation.
You examine Mrs Doolally and find that she has a GCS of 12/15 (Eyes = 3, Verbal = 4, Motor = 5). Her lung fields are clear, her abdomen is soft and non-tender, there are no signs of cellulitis or meningism, and she does not have a catheter or any lines in place. There are no signs of focal neurology and her pupils are equal and reactive to light.
What investigations would you request?
Septic Screen
Metabolic Screen
Toxicoloigy Screen
ECG
Describe the septic screen
Septic screen: full blood count (FBC), C-reactive protein (CRP), blood cul- tures, urine dipstick and urine MC&S, chest radiography.
− FBC: the white cell count (WCC) may be elevated if there is a systemic
infection. Anaemia could contribute to hypoxia.
− CRP: an elevated CRP points towards an inflammatory picture, although,
as with the WCC, it is non-specific regarding the cause.
− Blood cultures: these should be taken to look for infection and, if positive, to identify the organism and its sensitivity and resistance to various anti- biotics. However, they take time to come back so are of more relevance in
management than diagnosis.
− Urine analysis: it is important that this is performed on a mid-stream
urine (MSU) sample, in–out catheter sample, or suprapubic sample because the first part of a micturition stream will always be contaminated. Positive leucocyte esterase and nitrites indicate a UTI. A combination of positive glucose and ketones suggests diabetic ketoacidosis. A mid-stream sample can also be taken to look for specific bacteria.
− Urine microscopy, culture, and sensitivities (MC&S): as with the blood cultures, these should be taken to look for the offending organism if there are signs of infection on the urine dipstick.
− Chest radiograph: consolidation is seen in a chest infection. An enlarged heart would be suggestive, although not diagnostic, of heart failure, which could be the cause of cerebral hypoperfusion.
Describe the metabolic screen
• Metabolic screen: arterial blood gas (ABG), urea and electrolytes (U&Es), thyroid function, liver enzymes, thiamine, folate, vitamin B12:
− ABG: although you already have an idea of oxygen saturations from the
pulse oximeter, this would provide further information about hypercapnia and acid–base balance. Uraemia, diabetic ketoacidosis, and some toxins can cause metabolic acidosis.
− U&Es: a variety of different electrolyte imbalances can cause an acute con- fusional state, as can uraemia in renal failure.
2
2 − Thyroid function tests (TFTs): if clinical signs or the history suggests hypo- or hyperthyroidism, you should investigate T3/T4 and TSH levels. In some hospitals this is routinely performed as a first-line investigation in confused patients. − Liver function tests (LFTs): liver failure can result in a hepatic encepha- lopathy and is suggested by deranged LFTs. Abnormal LFTs, in particular a disproportionately raised gamma-glutamyl transferase (GGT), may point to alcohol abuse. − Thiamine, folate, and vitamin B12 levels: if you suspect the patient is mal- nourished, e.g. a homeless patient, an alcohol or drug abuser, or an eld- erly patient living alone who appears cachexic (such patients may live on a minimal ‘tea and toast’ diet), then look for a deficiency in thiamine, folate, and vitamin B12.
Describe the toxicology screen
• Toxicology screen: before requesting a toxicology screen, think of which drugs the patient will realistically have consumed. This is a labour-intensive and expensive test, and thus the biochemistry department will not thank you for ordering it without good reason. In an elderly patient like Mrs Doolally, alco- hol and prescription medications are likely candidates, whereas recreational drugs are unlikely.
Describe the ECG
• Electrocardiogram (ECG): an ECG should be done to exclude ischaemia or arrhythmia leading to a low-output state and hypoperfusion.
Mrs Doolally’s investigations were requested and she was found to have a raised WCC and ++ leucocyte esterase and +++ nitrites in her urine. Her other investigations were unremarkable.
In light of the history, examination, and investigations, what is the diagnosis?
The urine analysis confirms that Mrs Doolally has a UTI, even though clinically she had no suprapubic tenderness. It is not unusual for UTI to present without fever, espe- cially in the elderly who often have difficulty regulating their temperature. Moreover a significant number of patients take antipyretic medications such as steroids, mask- ing infections. It may appear odd that a ‘simple’ UTI could cause confusion, but you should think of how your own mental ability drops when you have a bad cold with a good going fever. That same drop in mental performance in someone who is already old and frail is why infections that may appear relatively trivial to young adults can cause acute confusion in the elderly. However, it is important to remember that UTIs are common in the elderly and may be coincidental. Therefore you must keep an open mind and be prepared to review the diagnosis if there is no response to treatment.
How would you manage Mrs Doolally acutely?
- Resuscitation: as with any acute presentation, you must first assess the need for resuscitation by examining the ABC.
- Antibiotics: check your local guidelines for which antibiotics to use for a UTI, as there are different patterns of resistance from common infective organisms (e.g. Escherichia coli) depending on where you practice.
• Confusion: there are a number of conservative measures you should take in confused patients:
− Ensure confused patients are not left unattended. Ideally they should be
cared for by the same nurse as this helps them orientate themselves in an
alien environment.
− Where possible, put them in a quiet side room.
− Discontinue non-essential medications as these may be contributing to the
confusion.
− Consider providing fluids and nutrition, as they may be unable or unwilling
to maintain a balanced intake. If you suspect thiamine deficiency second- ary to alcoholism or malnutrition, you must treat (e.g. with thiamine or Pabrinex, a cocktail of vitamins). Thiamine deficiency rapidly causes irre- versible cerebral damage and if you wait for the results of your investiga- tions it may already be too late.
• Sedation: If the patient becomes aggressive, you may have to resort to sedat- ing them. If so, you can give them:
− Haloperidol or chlorpromazine. These take about 30–60 minutes to take
effect and can have extrapyramidal side-effects; they are therefore to be
used with caution in Parkinson’s patients.
− Lorazepam. This acts more quickly, taking 5–10 minutes, and is useful in
restoring sleep. However, it may worsen confusion and is also a respiratory depressant.
In the longer term, the management of the confused patient involves treating the underlying cause of their confusion – in this case the UTI. Be wary of non-compliance in confused patients, particularly if they fail to respond to treatment.
Mr Hext is a 65-year-old man who is found to be confused on the ward round the day after resection of his colorectal cancer. His observations and investigations prior to the operation were all normal. There are no signs of infection on inspection of the wound site and he does not look or feel hot or sweaty. His peripheral pulses are present (if a little weak), lung fields are clear, there are no heart murmurs (to sug- gest endocarditis), and no obvious signs of infection elsewhere. He is not connected to a pulse oximeter, ECG, or blood pressure monitor so you ask for this to be done, and also order some investigations.
Given his history, what are the possible causes of his confusion that you should be thinking about?
Post-operative patients are commonly confused; this can be for any number of rea- sons related to their operation:
• Hypoxia: due to any combination of:
− anaemia from significant blood loss in surgery
− opiate analgesics leading to a depressed respiratory rate
− pulmonary embolism reducing gas exchange
− basalatelectasis
• Opiates: direct effect of opiate analgesics on their consciousness
• Electrolytes: derangement due to:
− intra- and post-operative fluid replacement
− lesscommonly,renalfailurecausedbyhypoperfusion
• Infection: unlikely in this case as there are no signs of infection on examination
• Sleep loss: hospitals are noisy and it is even harder to sleep if you are in pain.
Mr Burns is a 44-year-old man on the cardiac care unit who becomes confused and aggressive 4 days after suffering a myocardial infarction. Looking at his notes, you find nothing unusual in his observa- tions (pulse, blood pressure, temperature, blood glucose, oxygen saturation), drug history, or blood tests (including inflammatory markers, electrolytes, and liver function). However, you see in his initial clerking that he admitted to drinking 50–60 units a week and has a history of alcoholism.
What should you consider as a first step in this patient? What is the most likely diagnosis? What should you prescribe immediately?
First step: aggressive patients pose a risk to themselves, healthcare workers, and other patients. You should initially consider how to calm him down; if necessary, he may need sedation. However, you should be cautious about prescribing tranquiliz- ers too readily, particularly given the potential cardiac side-effects in a patient with ischaemic heart disease.
Diagnosis: having dealt with the immediate danger, you should proceed with investigating his confusion. The investigations already documented eliminate a number of possibilities. In a man with a history of alcoholism and a 4-day hospi- tal stay, alcohol withdrawal is the most likely candidate (severe cases are termed ‘delirium tremens’ and are associated with a high mortality). Such patients are at high risk of developing Wernicke’s encephalopathy due to thiamine deficiency, and this may potentially progress to permanent brain damage.
Immediate prescription: alcohol withdrawal is a medical emergency and can lead to fits and even death. You should prescribe thiamine immediately to pre- vent irreversible brain damage, and chlordiazepoxide (a sedative) to cope with the withdrawal.
Mrs Evans is a 47-year-old lady who is brought in by ambulance after her neighbour went around to check on her and found her ‘out of sorts’. You try asking Mrs Evans some questions and find her speech is unintelligible. Her neighbour says she lives alone and is self-sufficient, so there is no one to provide any detail as to how long this has been going on for. She does, however, say that she is a regular churchgoer and is teetotal.
Mrs Evans’ pulse is 72 bpm, blood pressure 131/83 mmHg, oxygen saturations of 98% on room air, res- piratory rate of 13/min, her temperature is 37.3°C. On examination, she is thin but not overly dishevelled, has no signs of a septic focus, and no asterixis. Her pupils are equal and reactive to light. A neurological examination reveals an intention tremor in both hands and significant ataxia such that she can barely stand or walk. Her GCS is 13/15 (Eyes = 4, Verbal = 3, Motor = 6).
You manage to speak to her daughter, who confirms her mother does not drink. She also tells you that she has suffered with bipolar disorder for over 20 years, for which she takes lithium. She is on no other medications.
You request a full set of bloods, including a metabolic and toxic screen, and ask the nurses to conduct a urinalysis when she next passes water. Her blood glucose is 4.2 mM, haemoglobin (Hb) 11.7 g/dL, WCC 4.1 × 109/L, CRP 2 mg/L, Na 132 mM, K 4.2 mM, Cl 101 mM, urea 12.3 mM, creatinine 143 μM, aspartate aminotransferase (AST) 23 U/L, alkaline phosphatase (ALP) 32 U/L, and her TFTs are within the normal ranges, as is her serum alcohol. A CT head scan shows no evidence of haemorrhage or any space- occupying lesion.
What other blood result would you like to know? What is the most likely diagnosis? What other mechanism(s) might be contributing to her confusion?
The differential diagnosis could still include an ischaemic stroke, less easily detected on CT than MRI, but given her relatively young age and the fact that she takes lithium, you should certainly order a lithium serum level.
Lithium toxicity could certainly account for both her confusion and renal impair- ment (as indicated by the raised urea; remember that urea rises out of proportion to creatinine initially because urea is normally reabsorbed in the proximal tubule, whereas creatinine is not). An alternative explanation for her urea and creatinine levels is dehydration. Mrs Evans also has mild hyponatraemia, but this is not suffi- cient to cause her confusion. Her lithium levels come back and are 3.7 mEq/L (nor- mal range 0.5–1.2).
Her renal compromise and slight uraemia could also be contributing to her con- fusion. Your priority should be to maintain her renal function whilst monitoring her lithium levels until they return to normal. In the longer term, her lithium dose may need changing, although you will also want to investigate her compliance (e.g. was she taking more than her usual dose because she felt down?).
Mrs Bright is a 54-year-old lady who is brought in by ambulance in the early hours of the morning after she was found by her husband wandering the streets. Her husband has come with her, although in her confused state she does not recognize him. She was reportedly behaving aggressively towards the paramedics but is now happy to be in the hospital. You find that she is not oriented in time and scores 5/10 on an AMTS. Her husband tells you that normally she is intellectually very capable (a crossword champion, no less!). He says she was perfectly fine when she went to bed and is distressed at the sud- den turn of events. When you ask him, he does recall that she had a headache before going to sleep for which she took paracetamol. She is otherwise fit and well and takes no regular medications. She has never smoked, is not diabetic or hypertensive, has no family history of note (both her parents died in old age), and is not known to have raised cholesterol.
Mrs Bright’s pulse is 109 bpm, blood pressure 121/78 mmHg, oxygen saturations of 98% on room air, respiratory rate of 12/min, her temperature is 40.3°C. On examination, she is alert with a GCS of 14/15 (Eyes = 4, Verbal = 4, Motor = 6). There is no dysarthria or impairment of sensation, limb movement, or vision, although she is photophobic and you therefore cannot perform fundoscopy. Her lungs are clear, there is no cellulitis, and no neck stiffness, rash, or herpetic lesions.
A CT is ordered and a lumbar puncture performed. The CT shows no signs of haemorrhage or raised intracranial pressure. The lumbar puncture shows an opening pressure of 28 cm, glucose 1.8 mM, pro- tein 3.2 g/L, WCC 1120/mm3 (90% neutrophils), red cell count 2/mm3, and Gram-positive intracellular diplococci.
What is the diagnosis?
Why were you interested in whether she smoked, was diabetic, hypertensive, had any family history, or high cholesterol?
Mrs Bright has meningococcal meningitis, based on the results of the lumbar puncture (very high WCC primarily neutrophils, Gram-positive intracellular diplo- cocci, protein >1 g/L, and CSF:blood glucose ratio <0.5, assuming blood glucose is in the normal range of 3.5–5.5 mM). Hers is an atypical presentation (mild head- ache and photophobia without neck stiffness or rash), but serves as a reminder that meningo-encephalitis can present in a variety of ways and that you should fully investigate a high fever.
Based on the history and examination (i.e. before you got the lumbar puncture results), a stroke was a possibility so you were interested in her risk factors as they inform about the likelihood of this. The lack of focal neurology makes a stroke less likely (and confusion is not a typical feature of stroke), and the CT helps exclude a haemorrhagic stroke.
Mr Clifton is a 59-year-old gentleman who is brought in by his son because he is ‘not himself’. You try asking him some simple questions but find his speech is unintelligible. His son tells you his father has his own business as an independent property lawyer and is usually ‘compos mentis’. They have din- ner together once or twice a week, the last time being before the weekend, 3 days ago, when he was perfectly fine. His medical history is notable for lung cancer, for which he is under the care of a multi- disciplinary team. His son says it has spread to the adrenals and that the prognosis is not good. He also comments that his father seems to have lost his appetite, which he attributes to a combination of the cancer and his medications, and has been increasingly tired, which he attributes to his low calorie intake. He cannot remember which medications his father takes. He says his father does not drink or smoke, but used to smoke 20 a day for 40 years.
His vitals are: pulse 96 bpm, blood pressure 98/58 mmHg, oxygen saturations of 99% on room air, respi- ratory rate of 12/min, temperature of 37.5°C. On examination, he is alert with a GCS of 14/15 but confused (Eyes = 4, Verbal = 4, Motor = 6). You note he has a dry tongue and no peripheral or pulmonary oedema. Chest and abdominal examination are otherwise unremarkable. There are no signs of focal neurology.
A bedside blood glucose and urinalysis are unremarkable. His bloods come back shortly after and show: Hb 13.4 g/dL, CRP 3 mg/L, Na 112 mM, K 6.2 mM, Cl 83 mM, urea 9.1 mM, creatinine 78 μM, AST 15 U/L, ALP 32 U/L, with TFTs pending. A toxic screen for alcohol is negative.
How should you investigate a patient with hyponatraemia?
Hyponatraemia is a common cause of acute confusion. Assuming Mr Clifton’s confusion is due to hyponatraemia, what is the likely underlying cause(s)? What should you be wary of when treating Mr Clifton?
High or normal serum osmolality indicates a ‘pseudohyponatraemia’, i.e. a low sodium result as an artefact. If the sodium is low, you would expect the overall osmolality to be low (given that sodium is the dominant ion that determines osmolarity). Some machines that measure sodium concentrations in laboratories assume a constant volume of water. If the serum is very concentrated, e.g. with protein or glucose, there will be less water in the vial and therefore less dissolved sodium. This gives rise to an artefactually low sodium reading. Curiously, blood gas analysers, such as those found on many acute wards, are not affected by this artefact.
Describe a true hyponatraemia
• If the patient has a low serum osmolality, i.e. a true hyponatraemia, you should work out whether they are hypervolaemic, euvolaemic, or hypovolaemic (this distinction is made largely on clinical findings):
− Hypervolaemic patients have signs of fluid overload, specifically peripheral
and pulmonary oedema and a raised jugular venous pressure (JVP). Hyper- volaemic hyponatraemia occurs in many conditions, including congestive cardiac failure, hepatic failure, and nephrotic syndrome.
− Hypovolaemic patients are dehydrated and have the corresponding signs, e.g. low blood pressure, tachycardia, dry mucous membranes, and decreased skin turgor. Hypovolaemia results in hyponatraemia as it stimulates secre- tion of antidiuretic hormone (ADH) in an attempt to retain fluid, thereby diluting sodium levels. A urine sodium will identify the site of sodium loss
as the kidney or elsewhere:
− urine sodium <220 mM indicates that the kidneys are responding normally
to a drop in circulating volume by concentrating the urine. This suggests an extra-renal source of sodium loss, e.g. from the gut (vomiting, diarrhoea), skin (sweating, burns), or into the peritoneal cavity (pancreatitis, small bowel obstruction);
− urine sodium >220 mM implies the kidneys are unable to concentrate urine normally and that salt is being lost in this manner. Causes include diuretics, renal failure, and mineralocorticoid insufficiency (Addison’s disease).
• Patients who have neither the clinical signs of hyper- or hypovolaemia should be considered euvolaemic. Measuring their urine osmolality will identify whether this is due to:
− the syndrome of inappropriate ADH secretion (SIADH), where excess
ADH allows water to re-enter the serum in the distal tubules impairing the ability of the kidneys to concentrate the urine, leading to a high urine osmolarity (>500 mmol/kg). Note that there are a number of other criteria that must be met before you can make a diagnosis of SIADH; or
− fluid overload (psychogenic polydipsia or iatrogenic), which would be acute, or severe hypothyroidism.
Describe the algorithm for hyponatraemia
See chart!
What is happening in Mr Clifton’s case
In Mr Clifton’s case, while lung cancer often causes SIADH (due to ectopic secre- tion of ADH by small cell lung cancers), the cause is more likely to be Addison’s disease. First, the hyponatraemia is hypovolaemic (low blood pressure, heart rate at the upper end of normal, no oedema). Although a urinary sodium has not been performed, his high potassium suggests this is due to a failure of the Na/K exchange mechanism in the distal tubule. This happens in adrenal insufficiency (Addison’s dis- ease), where a lack of mineralocorticoid (aldosterone) synthesis results in reduced Na/K exchange in the distal tubule with subsequent poor Na and water retention. The adrenals are a common site of metastases from the lungs, although it is unusual for this to result in an Addisonian picture.
You can confirm your hypothesis with a Synacthen test which, if he has Addison’s disease, will show no increase in cortisol after stimulation with adrenocorticotropic hormone (ACTH). It is important you perform a brief neurological examination on admission, including fundoscopy to look for signs of brain metastases, which could cause his confusion and may coexist with hyponatraemia.
The management of hypovolaemic severe hyponatraemia is a slow infusion of normal saline. You should be wary of correcting his hyponatraemia too rapidly, as this can cause central pontine myelinolysis and death. Thus, you should measure his serum sodium every 2–4 hours and, given this appears to have happened acutely (in the last 3 days), aim to increase his sodium by <2 mM/hour, and by no more than 10 mM/day. You can stop the infusion once he improves symptomatically, usually around 120 mM – there is no need to reach a sodium of 135 mM.
