jojo, on Mar 29 2008, 09:40 PM, said:
My husband has an incomplete spinal cord injury(central cord).
He took a fall last summer transfering into wheelchair and suffered
head injury. Since this trauma, we have set off this horrible syndrome.
Does anyone else have this, and what management program do you do.
JoJo
Hi JoJo,
Welcome,
before chair-landing-disability I trained and worked as a RN, I specialised in Cardiology but also worked in a variety of other areas too. So my experience in this instance isn't personal but is as the RN.
I have actually had more experience with Diabetes Insipidus ( not 'diabetic' as you would usually think of) and this is the other extreme to SIADH. To explain further, Lack of the hormone ADH = Diabetes insipidus (too much excretion of water), and too much ADH= SIADH - excessive retention of water by the body. The two are similar in that they are both Endocrine or Hormonal and both affect The posterior (back) lobe of the pituitary gland.
I am sorry if this is going over what you know already!
Info can be found here--->
HERE
Also below is an informative page/site on SIDAH:
http://www.patient.c...owdoc/40001100/
here is the info, I feel this is good info as it has some of the treatment options etc etc.:
Syndrome of Inappropriate ADH Secretion (SIADH)
PatientPlus articles are written for doctors and so the language can be technical.
SIADH is a rare syndrome of excessive or inappropriate secretion of vasopressin from either posterior pituitary or from ectopic sources such as small-cell lung cancer. Normally an increase in plasma osmolality (sensed in osmoreceptor cells) is the major stimulus to the secretion of vasopressin.1
SIADH is the commonest cause of hyponatraemia especially seen among the elderly. Total body sodium content is normal, but water is retained because elevated vasopressin (also called ADH - Anti-Diuretic Hormone) causes water absorption from renal collecting ducts despite continued fluid intake. It is characterized by2:
Hyponatraemia (serum sodium < 135 mmol/l)
Increased urinary sodium ( > 30 mmol/l)
Increased urine osmolality (>300 mOsmol/kg)
Absence of oedema or volume depletion
Normal renal, adrenal and cardiac function.
Presentation
The condition is asymptomatic during the initial stages, if the fall in the serum sodium level is slow. Rapid onset of hyponatraemia, rate of fall greater than 0.5 mmol/l/h, is associated with confusion, drowsiness, convulsions, coma and death. Symptoms are uncommon until the serum sodium falls below 120 mol/l, or the plasma osmolality drops below 268 mOsmol/kg. The cerebral oedema resulting from water intoxication causes the drowsiness, lethargy, irritability, mental confusion and disorientation, with fits and coma being the most profound features. Peripheral oedema is remarkably rare. Patients with SIADH continue to drink normal amounts of fluids despite low plasma osmolalities, due to a downward resetting of their osmotic threshold for thirst.3The major causes are:
CNS disorders - head injury, meningitis, encephalitis, brain tumour or abscess, haemorrhage, thrombosis, Guillain-Barre syndrome, acture intermittent porphyria.
Tumours - carcinoma (especially lung), lymphoma, leukaemia, thymoma, sarcoma, mesothelioma.
Respiratory disease - pneumonia, TB, emphysema, severe asthma, pneumothorax, positive-pressure ventilation.
Drugs - lithium, tetracyclines, carbamazepine, clofibrate, chlorpropamide, thiazides, phenothiazines, MAOIs, SSRIs, cytotoxics.
Hypotonic fluids in the post-operative state.
There is a rare inherited X-linked recessive type.4 5
Differential diagnosis
Renal and adrenal diseases can also cause high urinary sodium with low plasma osmolality. Hyponatraemia with a high plasma osmolality is caused by hyperglycaemia. Hypervolemic hyponatraemia may be caused by oedema-forming states such as congestive heart failure, liver cirrhosis, renal disease.
Hyponatraemia in CNS disorders may be due to cerebral salt wasting (CSW) which causes a contracted blood volume, whereas SIADH is a volume-expanded state. Accurate diagnosis is important because vigorous saline replacement and resuscitation is required for CSW, whereas fluid restriction is the treatment of choice for SIADH.
Investigations
U & Es, plasma osmolality, urinary sodium and osmolality. Adrenal and thyroid function (which should be normal).
Management
Withdraw drugs (such as lithium).
Fluid restriction to 500-750ml/day usually reverses any adverse clinical features and restores the circulating sodium level and osmolality to normal.
Demethylchlortetracycline (demeclocycline) 600 to 1200 mg daily which induces nephrogenic diabetes insipidus is often highly effective, making water restriction unnecessary (nausea, photosensitivity and diabetes insipidus can occur).
Hypertonic saline infusion (rarely required) in severe drowsiness and serum sodium <100mmol/l.
Plasma sodium should rise no faster than 0.5 mmol/l/hour and by no more than 12 mmol/l in the first 24 hours. Given under close supervision because over-rapid correction (especially in burn victims or the malnourished) can cause cardiac failure or cerebral oedema and pontine myelinolysis (spastic quadriplegia and pseudobulbar palsy).
Thiazide diuretics - enhance sodium excretion and water.
Vasopressin receptor antagonists are still experimental but represent a promising new treatment option.6
Document References
Warrell DA, et al. Syndrome of Inappropriate ADH Secretion. Oxford Textbook of Medicine, 4th Edition, Parts 12.3 and 12.12. Oxford University Press: 2003.
Baylis PH; The syndrome of inappropriate antidiuretic hormone secretion.; Int J Biochem Cell Biol. 2003 Nov;35(11):1495-9. [abstract]
Smith D, Moore K, Tormey W, et al; Downward resetting of the osmotic threshold for thirst in patients with SIADH.; Am J Physiol Endocrinol Metab. 2004 Nov;287(5):E1019-23. Epub 2004 Jun 22. [abstract]
OMIM - X-linked Nephrogenic Syndrome of Inappropriate Antidiuresis (NSAID)
Feldman BJ, Rosenthal SM, Vargas GA, et al; Nephrogenic syndrome of inappropriate antidiuresis. N Engl J Med. 2005 May 5;352(18):1884-90. [abstract]
Wong F, Blei AT, Blendis LM, et al; A vasopressin receptor antagonist (VPA-985) improves serum sodium concentration in patients with hyponatremia: a multicenter, randomized, placebo-controlled trial.; Hepatology. 2003 Jan;37(1):182-91. [abstract]
Acknowledgements EMIS is grateful to Dr Peter Kaye for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2007.
DocID: 813
Document Version: 20
DocRef: bgp1100
Last Updated: 15 Jun 2006
Review Date: 14 Jun 2008
I hope this is of use and perhaps others with a TBI will also have experiences to share with you.
Please do ask if there is anything unclear etc.
Best wishes,
Take care,
K
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