Ankle-brachial pressure index

The ankle-brachial pressure index is calculated by:

ABPI = (ankle systolic BP)/(brachial systolic BP)

Interpretation of results is not entirely straightforward as various consensus papers give different cut -offs for the definitions of 'moderate' and 'severe'.  One set of definitions is:

• >1.4: calcification may be present
• >1.0 probably no arterial disease
• 0.81-1.0 no significant arterial disease
• 0.5-0.8 moderate disease
• <0.5 severe disease
• <0.3 critical ischaemia

It is worth noting that an ABPI <0.9 or of >1.4 is an independent risk factor for cardiovascular disease.

ABPI may be non-diagnostic in patients with heavy arterial calcification, such as:

• diabetics (5-10% of diabetic patients cannot have their occlusive ankle pressure measured)
• the elderly
• renal failure

Reference
Al-Qaisi, M. et al. Ankle Brachial Pressure Index (ABPI): An update for practitioners. Vas Health Risk Manag. 2009; 5: 833-841.

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Driving rules UK

Key excerpts from the DVLA website (updated Sept 2012)

Rules:

• First unprovoked epileptic seizure/solitary fit (all attacks within one 24 hour period are treated as a 'single event') : 6 months off driving unless clinical factors suggest an unacceptably high risk of a further seizure.  For bus/lorry drivers: 5 years off.
• Known epilepsy: can drive whilst seizure free but:
• if a known epileptic has a seizure:
• during the day: 1 year off driving
• during the night: 1 year off driving unless they have had a seizure whilst asleep more than 3 years previously and no daytime attacks, in which case they may continue driving.
• cannot drive bus/lorry until off medication AND seizure free for 10 years
• Solitary loss of consciousness likely to be cardiac in origin (but excluding vasovagal collapses): 6 months off if no cause identified. 4 weeks off if cause identified and treated.
• TIA: no need to notify DVLA but must not drive for 1 month. For bus/lorry drivers: 1 year off.
• Stroke: must not drive for 1 month and may resume driving afterwards if satisfactory clinical recovery. For bus/lorry drivers: 1 year off.
• Unstable angina: must cease driving until symptoms controlled. No need to inform DVLA
• ACS: - no need to notify DVLA
• successfully treated by angio: can drive after 1 week as long as LVEF at least 40%
• can drive after 4 weeks if not successfully treated by angio
• if bus/lorry driver: at least 6 weeks off
• Elective PCI: no driving for 1 week. (6 weeks bus/lorry driver)  No need to notify DVLA
• CABG: no driving for 4 weeks, 3 months if bus/lorry driver.
• Pacemaker implant, including box change: no driving for 1 week (6 weeks for bus/lorry)

GMC advice: "if you do not manage to persuade the patient to stop driving, or you discover that they are driving against your advice you should contact the DVLA immediately and disclose any relevant medical information, in confidence, to the medical advisor. Before contacting the DVLA you should try to inform the patient of your decision to disclose personal information. You should then also inform the patient in writing once you have done so"

Reference:
DVLA: At a glance guide to the current medical standards for fitness to drive. Available at http://www.dft.gov.uk/dvla/medical/ataglance.aspx

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Lithium

Lithium is a drug with a narrow therapeutic window which is used predominantly in the treatment of bipolar disorder. 

It is predominantly renally excreted. 

Peak plasma levels usually occur between 0.5 to 4 hours but can occur up to 72 hours in case of overdose; steady state is achieved in 6 days.

Side effects of lithium include:

• Endocrinological 
• Thyroid dysfunction (both hypo and hyperthyroidism) 
• Hyperglycaemia 
• Hyperparathyroidism 
• Hypercalcaemia 
• Neurological
• Tremor 
• Gastrointestinal 
• Nausea/vomiting 
• Anorexia 
• Diarrheoa 
• Excessive salivation 
• Renal 
• Nephrogenic diabetes insipidus (20 to 70%) 
• Chronic renal failure 
• Proteinuria 
• Other 
• Alopecia 
• Metallic taste
• Leucocytosis 

Factors that predispose to lithium toxicity include 

• Increasing age 
• Anorexia 
• Diarrhoea 
• Vomiting 
• Dehydration 
• Hypertension 
• Heart disease 
• Renal impairment 
• Hypothyroidism 
• Drugs 
• ACE inhibitors 
• Diuretics 
• NSAIDs 
• Calcium channel blockers 
• Neuroleptics 
• Antiepileptics 

Symptoms of toxicity 

• Mild toxicity 
• Vomiting 
• Diarrhoea 
• Lethargy 
• Tremor 
• Drowsiness 
• Muscle weakness 
• Polyuria
• Polydipsia 
• Moderate toxicity 
• Confusion 
• Nystagmus 
• Cerebellar signs 
• Severe toxicity 
• Altered state of consciousness 
• Syncope 
• Seizures 
• Hyperreflexia 
• Arrhythmias 

The most common manifestation of toxicity is altered mental state. 

Investigations if toxicity is suspected:

• Lithium level – but note toxicity can occur within the therapeutic range
• Full set of bloods
• Calculate anion gap ( = Na – (Cl + HCO3) ) – look for a low anion gap 
• Calculate osmolar gap (= plasma osmolality – ((2xNa) + plasma glucose + urea) ) – look for an elevated osmolar gap 

Management

• Manage airway as appropriate 
• Gastric lavage if OD less than 1 hour previously 
• ?whole bowel irrigation if large quantities of slow-release tablets swallowed
• IV saline if volume depleted
• haemodialysis 

References
BNF. Lithium. Accessed 22/5/12 at http://www.bnf.org/bnf/index.htm 
Delva, N. and Hawken, E. Preventing lithium intoxication. Guide for physicians. Can Fam Physician. 2001; 47: 1595-1600.
MHRA. Lithium overdose. Accessed 22/5/12 at http://www.mhra.gov.uk/Howweregulate/Medicines/Licensingofmedicines/Informationforlicenceapplicants/Guidance/OverdosesectionsofSPCs/Genericoverdosesections/Lithium/index.htm 
Sood, M. and Richardson, R. Negative anion gap and elevated osmolar gap due to lithium overdose. CMAJ. 2007; 176(7): 921-923.

Timmer, R. and Sands, J. Lithium intoxication. J Am Soc Nephrol. 1999; 10(3): 666-674.

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Cavernous Sinus Syndrome

Cavernous sinus syndrome is a syndrome characterized by neuropathies of the cranial nerves passing through the cavernous sinus. 

The nerves passing through the cavernous sinus are:

• Occulomotor (III) 
• Trochlear (IV) 
• Ophthalmic (V1)
• Maxillary (V2) 
• Abducens (VI) 

The optic nerve (II) runs just above the cavernous sinus. 

A diagram illustrating the anatomy of the cavernous sinus is shown below: 

Presentation of cavernous sinus syndrome is with palsies of whichever cranial nerve is affected, such as impairment of eye movement or Horner’s syndrome. 

Causes of cavernous sinus syndrome include: 

• Infection 
• Bacterial – staph, strep, tuberculosis 
• Fungal 
• Viral 
• Vascular 
• Aneurysm of internal carotid artery 
• Thrombosis 
• Inflammation 
• Sarcoidosis
• Toloso-Hunt syndrome 
• SLE
• Neoplasia 
• Pituitary adenoma
• meningioma 
• mets – especially nasopharangeal carcinoma, lymphoma, meningioma, lung and breast metastases 

Treatment depends on the cause. 

References

Lee JH, et al. Cavernous sinus syndrome: clinical features and differential diagnosis with MR imaging. AJR Am J Roentgenol. 2003; 181(2):583-90. 

Sharkawi E, Tumuluri K, Olver JM. Metastastic choriocarcinoma causing cavernous sinus syndrome. Br J Ophthalmol. 2006; 90(5): 654-5. 

Zarei M, Anderson JR, Higgins JN, Manford MR. Cavernous sinus syndrome as the only manifestation of sarcoidosis. J Postgrad Med 2002;48:119

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Gitelman syndrome

Gitelman syndrome is an autosomal recessive condition characterised by hypokalaemia and hypomagnesaemia.

It is caused by mutations in the genes coding for the NaCl and Mg transporters in the distal tubule resulting in decreased sodium and magnesium reabsorption.

Presentation:

• Lethargy
• Muscle cramps 
• Weakness 
• Hypotension/normal blood pressure 

Biochemically: 

• Hypokalaemia 
• Hypomagnesaemia
• Hypocalciuria 
• Metabolic alkalosis 
• Hypereninaemic hyperaldosteronism 

Treatment:

• Potassium replacement 
• Magnesium replacement 
• Amiloride 

References: 

Graziani, G. et al. Gitelman syndrome: pathophysiological and clinical aspects. QJM. 2010; 103(10): 741-748. 

OMIM: Gitelman syndrome. Available at http://omim.org/entry/263800?search=gitelman&highlight=gitelman.

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Bartter’s syndrome

Bartter’s syndrome is an autosomal recessive condition which results in severe hypokalaemia.

It is caused by defective chloride ion reabsorption in the Na-K-2Cl channels in the loop of Henle. 

It presents in early childhood with:

• Failure to thrive 
• Polyuria 
• Polydipsia 

Note blood pressure is normal (in contrast to Liddle’s syndrome, in which it is high)

Biochemically there is: 

• Metabolic alkalosis 
• Hypokalaemia 
• High urinary potassium and sodium
• Hypercalciuria 
• Hyperreninaemia 

Treatment: 

• Potassium replacement 
• NSAIDs – usually indomethacin 

Patients who are untreated may have a slightly lowered IQ.

References:

Amirlak, I. and Dawson, K. Bartter syndrome: an overview. QJM. 2000; 93(4):207-215. OMIM: Bartter Syndrome. Available at http://omim.org/entry/601678?search=bartter&highlight=bartter.

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Liddle syndrome

Liddle syndrome is an autosomal dominant condition characterised by hypertension and usually hypokalaemia. 

It is caused by increased sodium reabsorption in the distal convoluted tubule. 

Biochemically: 

• Hypokalaemia
• Metabolic alkalosis 
• Low plasma renin 

Treatment 

• Salt restriction 
• Potassium replacement 
• Amiloride 

References:

OMIM: Liddle syndrome. Available at http://omim.org/entry/177200?search=liddle&highlight=liddle 

Warnock, D. Liddle syndrome: an autosomal dominant form of human hypertension. Kidney Int. 1998; 53(1): 18-24.

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