Investigations
1st investigations to order
venous blood gas
Test
May show:
Respiratory alkalosis in patients with alcohol withdrawal delirium (also known as delirium tremens) due to significantly elevated cardiac indices, oxygen delivery, and oxygen consumption[97]
Hyperventilation and consequent respiratory alkalosis with alcohol withdrawal delirium may result in a significant decrease in cerebral blood flow[97]
Hypochloraemic metabolic acidosis with vomiting[98]
Metabolic acidosis with a high anion gap if alcohol ketoacidosis is present. This is a potential cause of alcohol withdrawal as well as a differential diagnosis.[99]
Result
respiratory alkalosis
hypochloraemic metabolic acidosis
metabolic acidosis with a high anion gap
blood glucose
Test
Hypoglycaemia is common in patients with alcohol dependence or withdrawal and may be secondary to poor nutrition or heavy alcohol use.
Replace glucose orally if tolerated or intravenously if the patient has impaired consciousness. Consider intramuscular glucose if venous access is unavailable.
If you give glucose, give it at the same time or after thiamine. However, do not delay glucose for life-threatening hypoglycaemia while waiting for thiamine administration.
Result
hypoglycaemia
full blood count
Test
Increased mean corpuscular volume (MCV) is indicative of chronic alcohol-use disorder.[5]
May remain elevated 3 to 4 months after the patient stops drinking alcohol.
Not a specific test; can be elevated as a result of vitamin B12 or folate deficiency.
Thrombocytopenia in patients with alcohol-use disorder is caused by splenomegaly, folate deficiency, and, most frequently, a direct toxic effect of alcohol on production, survival time, and function of platelets.[103]
Generally benign; clinically significant haemorrhage is rare.[103]
Result
increased MCV
thrombocytopenia
urea and electrolytes
Test
Electrolyte deficiencies are common in people with chronic alcohol-use disorder.[104]
They can cause life-threatening cardiac arrhythmias; always perform an ECG on patients with electrolyte deficiencies.[105][106][107][108]
In those admitted to hospital with chronic alcohol-use disorder, plasma magnesium, potassium, and phosphorus concentrations may be normal or only slightly reduced on admission, only to decrease over several days. This is due to an inward cellular shift that unmasks decreased total-body stores[104]
Hypomagnesaemia: occurs in almost one third of people with chronic alcohol-use disorder[104]
Practical tip
Hypocalcaemia and hypokalaemia will not resolve until adequate magnesium replacement is given.[109]
Hypokalaemia: seen in nearly 50% of hospitalised patients with chronic alcohol-use disorder[104]
Results from inadequate intake and gastrointestinal losses due to diarrhoea. Urinary losses also contribute.
Hypophosphataemia (refeeding syndrome): develops in up to 50% of patients hospitalised for problems related to chronic alcohol overuse[104]
Result
hypomagnesaemia
hypokalaemia
hypophosphataemia
liver function tests
Test
Liver enzymes (aspartate aminotransferase [AST], alanine aminotransferase [ALT], and gamma-glutamyl transpeptidase [GGT]) may be elevated.[110]
ALT: almost always elevated, and normally higher than AST, in patients with alcoholic liver disease. The classic ratio of AST:ALT >2 is seen in about 70% of patients.[110]
GGT: may be increased with heavy alcohol consumption.[111]
Usually returns to normal levels within 2 to 3 weeks after the patient stops drinking alcohol if there is no chronic liver damage[111]
GGT greater than 10 times the upper limit of normal is commonly associated with excessive drinking.[112] Smaller elevations of GGT (e.g., 2-3 times the upper limit of normal) tend to be caused by other conditions including non-alcoholic fatty liver disease.[113]
Result
elevated liver enzymes (AST, ALT, and GGT)
bone profile
Test
Use to detect:
Result
hypocalcaemia
low vitamin D
coagulation studies
Test
International normalised ratio (INR) and prothrombin time (PT) may be prolonged in chronic liver disease.[114]
They correlate well with the severity of liver disease but are not predictive of bleeding risk.
Activated partial thromboplastin time (aPTT) does not usually reflect liver dysfunction; is typically normal or nearly normal in liver disease.[114]
Result
prolonged INR and PT in chronic liver disease
Investigations to consider
blood cultures
Test
Request in patients who are febrile to look for evidence of infection.[115]
Result
positive if infection present
CT head
Test
Request in patients with any one of:
Use the Glasgow Coma Scale (GCS) to assess conscious level [ Glasgow Coma Scale Opens in new window ]
Suspected head injury plus one of the following:[36]
GCS <13 on initial assessment
GCS <15 at 2 hours after the injury on assessment
Suspected open or depressed skull fracture
Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ears or nose, Battle’s sign)
Post-traumatic seizure
Focal neurological deficit
>1 episode of vomiting.
Practical tip
Always suspect head injury in patients who are withdrawing from alcohol; have a low threshold for requesting a CT head. Alcohol intoxication is an independent risk factor for a positive finding on CT head following head injury.[116] Patients who drink heavily are more likely to bleed after a head injury due to deranged clotting and thrombocytopenia.
Result
positive if significant head injury
chest x-ray
ECG
Test
Perform in patients with tachycardia to look for arrhythmias.
These include atrial fibrillation (AF) and ventricular tachyarrhythmias.[119]
Result
tachyarrhythmias (including AF and ventricular tachyarrhythmias)
amylase/lipase
ammonia
lumbar puncture
Test
Perform a lumbar puncture if you suspect subarachnoid haemorrhage (SAH) and the initial CT head is normal or if you suspect central nervous system (CNS) infection.[57][123]
Consider CNS infection or SAH if symptoms of confusion are worsening or failing to improve despite treatment for alcohol withdrawal, especially if the patient has a headache, fever, or neck stiffness.
Treat empirically if there is diagnostic uncertainty before waiting for lumbar puncture results.[124]
Result
positive in CNS infection or SAH
electroencephalography (EEG)
Test
Perform in all patients with first presentation of an alcohol withdrawal seizure or when there is a new seizure pattern in patients with a known history of alcohol‐related seizures (e.g., focal seizures or status epilepticus).[58]
Use EEG to help confirm the seizure has ended, particularly if you suspect ongoing subtle seizures in an unresponsive or anaesthetised patient.[58]
The incidence of EEG abnormalities is lower with alcohol withdrawal seizures (AWS) than other causes of seizures.[3]
Do not perform an EEG if the patient has had previous comprehensive investigation of their seizures and the pattern of current seizures is consistent with past events.[58]
Practical tip
Access to EEG is limited and it is not commonly used outside of the intensive care setting.
Evidence: Use of EEG in alcohol withdrawal seizures
There is limited evidence to support either the use of EEG in alcohol withdrawal seizures or the notion that EEG monitoring independently improves outcome in convulsive status epilepticus (SE).
Result
may be normal in alcohol withdrawal seizures
abnormalities (slow or epileptiform activity) suggest that the seizure may be due to other causes apart from alcohol withdrawal[3]
blood-borne virus screen
Test
Order if you suspect hepatitis B, hepatitis C, or HIV infection in the history or on examination.
Result
positive if hepatitis B, hepatitis C, or HIV present
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