A slim, unkempt girl, probably in her 20’s, presented to ED following a seizure. She has a further generalised tonic-clonic seizure in ED, which self-terminates prior to any drug therapy. Whilst she remains post-ictal she has a series of investigations performed including an arterial blood gas. She is referred to ICU immediately the blood gas result is obtained.
[az_accordion_section] [accordion title=”Question 1″ id=”acc-1″]What are the main abnormalities in the blood gas?[/accordion] [accordion title=”Question 2″ id=”acc-2″]Can you provide an explanation for these?[/accordion] [accordion title=”Question 3″ id=”acc-3″]Are there any specific physical signs you would look for to support your initial diagnosis?[/accordion] [accordion title=”Question 4″ id=”acc-4″]Are there any other investigations, apart from serial blood gases, that you would like?[/accordion] [accordion title=”Question 5″ id=”acc-5″]Does this patient need admission to ICU/HDU and if so, what would your ongoing management for her be?[/accordion] [/az_accordion_section]
- What are the main abnormalities in the blood gas?
Hyponatraemic hypochloraemic metabolic alkalosis with renal impairment.
- Can you provide an explanation for these?
The most likely diagnosis is bulimia nervosa, given the history of a slim young girl with a data set that suggests recurrent vomiting, which is typically part of the eating disorder that is characterised by binge eating with associated behaviours aiming to prevent weight gain, such as self-induced vomiting (H+ and K+ loss), misuse of laxatives or diuretics (HCO3- and K+ loss). These behaviours can lead to hypovolaemia and dehydration, resulting in hypotension, tachycardia and renal impairment.Patients with bulimia are often not slender, however, and are more commonly of average or slightly overweight build. Conversely, individuals with anorexia nervosa tend to be slim, or in severe cases, cachectic. However, the metabolic disturbance in this case suggests recurrent vomiting, which is more characteristic of bulimia as they seek to eliminate ingested food, while anorectics try to avoid consuming it in the first place. Other differentials to consider include pregnancy related conditions such as hyperemesis gravidarum, HELLP syndrome and ecclampsia, along with standard pathologies such as cholecystitis and alcoholism.
- Are there any specific physical signs you would look for to support your initial diagnosis?
There are no specific physical signs to support the presumed diagnosis of bulimia nervosa. The presence of erosion of dental enamel may indicate recurrent vomiting. Parotid enlargement may be subtle. Russell’s sign, namely calluses on the knuckles or back of the hand may support the suggestion of repeated self-induced emesis. The calluses appear from the repeated contact of the knuckles with the incisor teeth during the intentional inducing of the gag reflex at the back of the throat.Look also for features of depression and distorted body image. In severe cases, associated physical signs include hypothermia, relative hypotension and/or tachycardia, dry skin, lanugo (soft and fine) hair on the face and body.
- Are there any other investigations, apart from serial blood gases, that you would like?
In the setting of a presumed first presentation seizure, a CT brain is required, to exclude an intracranial pathology. In the absence of any identifiable intracranial pathology, it would be reasonable to assume that the aetiology of the seizures is the metabolic disarray. Other investigations in addition to the bloods already obtained would include:
- Full blood count: Not least to exclude an anaemia due to nutritional deficiency and a haematological malignancy. The WBC may be marginally elevated or depressed, even in the absence of sepsis
- Clotting profile: potentially a vitamin K deficiency causing an abnormal result
- Phosphate, magnesium: commonly deplete (Beware of refeeding syndrome in severe cases)
- Liver function tests
- Complete endocrine profile, including thyroid function, adrenal cortical & gonadotropin hormones
- Urine for electrolytes and drug screen, including diuretics and laxatives
- B-hCG to exclude pregnancy in any woman of child bearing age who presents with vomiting (hyperemesis, cholecystitis, appendicitis), metabolic derangement (HELLP syndrome) or seizure (eclampsia). If positive, needs a pelvic U/S to identify an ectopic gestation
- Does this patient need admission to ICU/HDU and if so, what would your ongoing management for her be?
Given the presumed aetiology of the seizure being due to hyponatraemia, it is necessary to admit this girl to HDU/ICU for ongoing monitoring and management of the electrolyte disturbances. In addition to slowly correcting the hyponatraemia and hypochloraemia, it will be vital to rehydrate her, given her renal dysfunction.
Whilst rapid correction of hyponatraemia is generally considered dangerous, given the potential for central pontine myelinolysis (CPM); in the setting of symptomatic hyponatraemia (continuing or recurrent seizures), it may be necessary to carefully raise the serum sodium concentration. It is important to note that the patient, a young female, is at particular risk of CPM. CPM is most likely to occur when rates of correction exceed 12 mmol/litre per day, but has occurred with corrections of only 9 mmol/l in 24hrs. Additionally, the seizure threshold will be reduced after increases in serum sodium concentrations of only 3-7 mmol/l.
The use of hypertonic saline is warranted to correct the sodium concentration. The rate will in part depend on the concentration used, namely 1.8%, 3% or 5%. I would initially use 3ml/kg of 3% saline over 10 – 20 minutes for cessation of hyponatraemic seizures. My goal would be to terminate the seizures and then slowly raise the serum sodium concentration by 4mmol over the first 8 hours of treatment, and then reduce the rate of rise, to achieve a maximum rise of 8mmol/l over 24hrs. Consequently, my approach in this particular case would be, following the initial bolus of hypertonic saline, to use 0.9% saline and regular serum EUCs to monitor the rate of serum sodium rise.
Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med 2000; 342:1581-1589
Feel free to discuss this case in the ICN Forumor post a comment below.
A new Case of the Month will be published soon.