# it is complication of type 1 DM And rare in type 2 dm
#precipitating factors are too little or no insulin ,infections and stress

## pathogenesis

d k a results from insulin defiagency and glucagon excess

** 1 consequences of insulin def.
1 hyperglycemia resulting in hyperosmolar state which induces osmotic diuresis leading to volume depletion and dehydration
2 activation of lipolysis in + tissue resulting in increasing amounts of free fatty acids into plasma which is taken by lives

** 2 consequences of glucagon excess
1 increased hepatic gluconeogenesis and impaired peripheral utilisation of glucose both resulting in sever hyper glycemia - osmotic diuresis -volume depletion and dehydration
2 activation of Ketogenic process resulting in ketosis and metabolic acidosis
3 two strong acids acetoacetic acid and beta hydroxybuturyic acid are responsible for the acidotic states - acids dissociates - releasing hydrogen ions - fall in ph

## clinical features
* D k a begins with anorexia vomiting and increased state of urine formation
* abdominal pain is dominant feature
* ultered consciousness or frank coma occure in untreated cases
* kussmauls breathing and a fruity odour due to acetone
* signs of volume depletion and dehydration
* leucocytosis is feature of d k a  per se and may not indicate infection

## complications

1acute gastric dilation or erosive gastritis 2 cerebral oedema 3 hyperkalaemia 4 hypoglycemia 5 insulin resistance  6 myocardial infraction 7mucormycosis 8 ards and vascular thrombosis

## investigation

1urine examination shows glucose and ketones
2 plasma glucose levels are raised  often markly
3 plasma ketone values are raised
4 potassium levels are normal or  raised initial stages  drops when treatment started
5 sodium levels are usually low
6 bicarbonates levels are low
7 hydrogen ion levels of blood are raised
8blood urea nitrogen  levels are raised

## management
 vital signs  urine out put and blood chemistry  charts are maintained
#1 insuline
d k a treated with regular insuline     i v may also be i m but neve7 subcutaniously

#2 fluid replacement
1 the usual fluid deficit is 3 -5 lit
should be given by i v
2when plasma glucose falls below 250mg /dl glucose saline solution should be given

#3 potassium replacement
1 initially levels are high when levels falls after starting treatment levels falls potassium suppli. Started at this stage
#4 bicarbonate therapy this is initialed only in severe acidosis (ph less than 7) especialy if hypotention is present
it should be given as infusion of isotonic of sodium biacarbonates (1.4%)
Infusion should be stopped when ph reaches 7.2


major cause of death are m i and infection perticularly pneumonia and cerebral oedema in children
poor prognostic signs are hypotention, azotaemia ,deep coma and associated illness

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