Dear Editor

It is not clear in this article how the conceptual leap from some of the knowledge tested to inability to care for critically ill patients has been made. Does not knowing the survival rate of patients suffering a cardiac arrest, for example, or the role of the bag attached to a non-rebreathing oxygen mask really compromise patient care?

From the limited results presented, there is no data whatsoever to suggest that any of the specific areas of knowledge tested have any bearing on safety. The fact that SHOs seem to know even less in some respects than PRHOs supports this.

If the authors believe that patient safety is compromised by not knowing what the bag does on an oxygen mask, they should perhaps audit morbidity and mortality outcomes before and after providing instruction.

Sir- Shah and colleagues report (1) about the prevalence of psychiatric disorders affecting elderly people institutionalised in a rehabilitation unit, concludes about depression that it is common among older adults, it is a treatable condition and that in cases which there are cognitive impairments associated to concomitant depression, the cognitive impairments are worsened by the depressive disease. Although the relevance about the high prevalence of cognitive impairments and depression in these patients is important and it is necessary to call attention on it, I believe that from the psychiatric perspective, the problem has been oversimplified. Therefore, we cannot accept the Shah et al elementary proposition about a drug trial with the selective serotonin reuptake inhibitors (SSRI’s) to elucidate the correct diagnosis when diagnostic doubts remain.

Depressive states in older patient groups have a tremendous clinical heterogeneity. Besides the depressive elderly patient without complicated somatic pathology or psychiatric co-morbidity, which will respond usually to antidepressant drugs, a significant proportion of other symptomatic depressed patients (whose cases are precisely studied by Shah and colleagues in this article) should be considered into the following distribution : A first subgroup of elderly depressed patients, may show greater cognitive deficits as compared to age-similar normal subjects (2) . These patients also present (subcortical) dysfunction of learning and memory, comprising the so-called "depressive pseudodementia", and may show reversible cognitive deficits after successful somatic treatment of depression. A second patients subgroup, display cognitive deficits characterised by severe prefrontal dysfunction, with perseveration, psychomotor retardation and long P300 latency (3) . A third subgroup, presents features of depression that are related to underlying vascular disease and neurological lesions, corresponding to the hypothesised "vascular depression" (4). In the fourth place, many patients with late- life onset of cognitive deficits, psychomotor retardation and limited depressive ideation, correspond to the "apathy syndrome (5) " that frequently follows brain damage in caudate, putamen and thalamus, usually secondary to cerebrovascular heterogeneous diseases.

While SSRI’s may be useful for the first subgroup, they are useless in the second and third one, while in the fourth, the dopamine agonists like bromocriptine are required. Hence, it is erroneous to overgeneralise that "depressed elderly respond well to SSRI’s" like Shah et al suggest. And what about the caution needed in the SSRI’s prescription (where Shah and colleagues state that these drugs are safe in the elderly, in spite of their habitually need of multiple medications) because of its significant drug interactions resulting from interference with components of the hepatic "P-450 enzyme system" (6)?.

Moreover, Shah and colleagues also state that patients with dementia may become depressed, particularly if they have insight into their condition. Evidence based medicine shows that the frequent depressive symptoms founded in these patients, are indeed early manifestations of Alzheimer disease (7), in which case, cholinesterase inhibitor drugs instead antidepressants is indicated.

Incidentally, Shah and colleagues state that there are no biological diagnostic tests for depression. Besides the dexametasone-cortisol test, the high prevalence of brain dysfunction in the geriatric depressed and cognitive impaired patient suggests that the computer analysed, quantitative electroencephalographic record (QEEG) may help not only in the brain damage differential diagnosis but also in signalling depressive disease by showing the characteristic increased anterior alpha power and decreased generalised coherence (8).

Drug treatments for every elderly disturbance, like for any other human complaint, must to be always a carefully skilled decision.

1.- Shah DC, Evans M, King D. Prevalence of mental illness in a rehabilitation unit for older adults. Postgrad Med 2000 ; 76 : 153 - 156

2.- Kramer-Ginsberg E, Greenwald BS, Krishnan RR, Christiansen B, Hu J, Ashtari M et al. Neuropsychological Functioning and MRI Signal Hyperintensities in Geriatric Depression. Am J Psychiatry 1999 ; 156 : 438 - 444

3.- Kalayam B, Alexopoulos GS. Prefrontal Dysfunction and Treatment Response in Geriatric Depression. Arch Gen Psychiatry 1999 ; 56 : 713 - 718

4.- Alexopoulos GS, Meyers BS, Young RC, Campbell S, Silbersweig D, Charlson M. Vascular Depression Hypothesis. Arch Gen Psychiatry 1997 ; 54 : 915 - 922

5.- Marin RS. Apathy : a neuropsychiatric syndrome. J Neuropsychiatry Clin Neurosci 1991 ; 3 : 243 -254

6.- The P-450 System : Definition and Relevance to the Use of Antidepressants in Medical Practice. Arch Fam Med 1996 ; 5 : 406 - 412

7.- Chen P, Ganguli M, Mulsant BH, DeKosky ST. The Temporal Relationship Between Depressive Symptoms and Dementia. Arch Gen Psychiatry 1999 ; 56 : 261 - 266

8.- Hughes JR, John R. Conventional and Quantitative Electroencephalography in Psychiatry. J Neuropsychiatry Clin Neurosci 1999 ; 11 : 190 - 208

A recent review article in your journal gives the impression that the case for heparinisation of patients with cerebral venous thrombosis (CVT) is proven [1]. The largest and most robust study did not come to this conclusion and its results did not achieve statistical significance [2]. Given that CVT has a spectrum of presentations from headache to coma, a blanket approach to treatment in the absence of good evidence and continued debate [3] does not seem sensible.

1. Allroggen H, Abbott RJ. Cerebral venous sinus thrombosis. Postgrad Med J 2000;76:12-15.

2. de Bruijn SF, Stam J, for the CVST Study Group. Randomised, placebo-controlled trial of anticoagulant treatment with low-molecular- weight heparin for cerebral sinus thrombosis. Stroke 1999;30:484-488.

3. Lewis MB. Cerebral venous thrombosis: nothing, heparin, or local thrombolysis? Stroke 1999;30:1729.

Dear Sir,

This case is extremely useful as an illustration of the varying presentations of phaeochromocytomas. The inclusion of the CT and the details of the differential effects given depending upon the catecholamine released were helpful.

I might venture a further, perhaps more important, mediator of the dramatic drop in K+ noted in this patient and other phaeos. There are a large number of beta adrenoceptors and sympathetic nerves in the renin- secreting apparatus of the kidney. Stimulation of these should precipitate, eventually, a raised aldosterone level and thus a drop in K+ (with an increased Na+). Neither Na+ nor any of the components of this renin-(ACE)-AGII-Aldosterone axis were measured in the article. I wonder what any relevant tests actually did show? When discussing how beta- blockers work in hypertension, this is undoubtedly part of the wider explanation.