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* Causes of hyponatraemia with increased ECV:
1- Heart failure
2- liver failure
3- Hypoalbuminaemia
4. Oliguric renal failure
5. Drugs (e.g. carbamazepine)
6. Hyperlipidimia (pseudohyponatreamia)
* Clinical features of hyponatraemia:
Mainly neurological symptoms appear when Na level < 120meq\l,
headache, confusion, restlessness leading to drowsiness, myoclonic
jerk, generalized convulsion and coma.
** Treatment:
1- It should be by slow correction, less than 0,5meq\l\ hour to avoid
central pontine myelinolysis.
2- Isotonic saline is the treatment of choice for hyponatraemia with
low ECV.
3- Water restriction is the primary treatment for hyponatraemia with
normal or increased ECV.
4- Treatment of the cause:- for example
a- Hormonal replacement in case of adrenal hypo function.
b- Demeclocycline,which is drug that antagonizes antidiuretic
hormone (ADH) activity at renal tubules in patient with syndrome
of inappropriate antidiuretic hormone secretion (SIADH).
c- The amount of NaCl necessary to raise plasma Na level to
desired value:- Na deficit = TBW X (desired Na – present Na).
d- Example: - A lethargic woman of 80 Kg body weight found to
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have plasma Na of 118meq\l, How much NaCl must be given to
raise her plasma Na to 130meq\l?
Na deficit =TBW X(130-118)
TBW is approximately 50% of body weight in the female, so:
Na deficit =80X 0.5 X(130-118) = 480meq.
e- Since normal ( isotonic ) saline contains154meq\l,the patient
should receive 480\154meq\l or 3.12 L for correction rate of
0.5meq\l\hour,this amount of saline should be given over
24hours (130ml\h).
B- Hypernatraemia: Is defined as serum Na >145meq\l
* Causes:
1- Central diabetes insipidus.
2- Nephrogenic diabetes insipidus.
3- Administration of hyper tonic saline
4 - Use of NaHco3 in large amount.
5- Use of Na-containing-drugs in large dose (e.g. NSAID; some
antibiotic).
* Clinical features:
Symptoms:-
1. Nausea, 2. Vomiting, 3.Fever and confusion. 4. History of long
standing 5. Polyuria, polydepsia and thirst. 6. History of drugs use.
Signs:
Restlessness, flushed skin, sticky mucous membrane, swollen red
tongue.
* Treatment:
1. The correction should be done over 48h to avoid cerebral oedema.
(By decreasing the Na level by <10 meq\l\24h ).
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2. Treat the underlying cause e.g. in case of central diabetes insipidus,
replacement of ADH in form of desmopressin
3. Hypernatraemia with low ECF is generally corrected with
hypotonic solution such as 5% dextrose in water over 24h, but
before that we have to restore plasma volume to normal by isotonic
fluids.
4- Hypernatraemia with increased ECF should be treated with a loop
diuretics along with I.V 5% dextrose in water.
Example:
- 70 Kg man is found to have a plasma Na of 160meq\l, what is his
water deficit ?
- if one assume that the hypernatraemia is from water loss only, thus
assuming he had normal Na level of 140meq\l and TBW is 60% of
body weight: Normal TBW X 140 = present TBW X Na level.
(70X 0.6 )X 140 = present TBW X 160 present TBW = 36.7 L
water deficit = normal TBW- present TBW = (70 X 0.6 ) - 36.7 =
5.3 L.
- to replace this deficit over 48 h, one would give 5% dextrose in
water intravenously,5300ml over 48 h, or 110 ml \ h.
Serum Potassium level disturbances:
- Abnormalities in K level are among the more common electrolyte
disturbance encountered in clinical medicine.
- Hypo and hyperkalaemia can cause life-threatening dysarrhythmias
C- Hyperkalaemia:
1- It is defined as serum potassium ( K ) level > 5m.mol\l.
2- Sever hyperkalaemia is considered when serum K level >7m.mol\l
and \or presence of ECG changes.
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3- The main causes of Hyperkalaemia:
a- Increased intake: e.g. I.V fluids, rapid massive blood transfusion.
b- Decreased excretion: e.g. use of ACE inhibitors, aldosterone
deficiency, K-sparing diuretic and renal failure.
c- Extra cellular redistribution e.g. diabetic ketoacidosis, cellular
destruction(haemolysis),use of B-blocker.
4- The clinical manifestations of Hyperkalaemia are: They mainly
involve the neuromuscular (N.M) and cardio-vascular (C.V) systems.
* C.V.System changes:
a- Dysarrhythmias..….a systole, heart block
b- ECG changes:
- Tall peaked T-wave, Prolonged PR-interval Decreased P- wave
amplitude. QRS –widening.
* N.M changes:
- Paraesthesia, weakness, paralysis, confusion.
5- Treatment of hyperkalaemia:
1- Eliminate the cause e.g. stop K intake.
2- Calcium salts which antagonize the action of K on the heart,
e.g. Ca gluconate (10%) 10ml I.V which has immediate effect.
3- Transfer the K into the cells:-
4. Insulin\glucose ( 50g +10-20 units crystalline insulin I.V )
5. B-receptors stimulants e.g. salbutamole.
6. Na-Hco3, ( 50-100 mmol I.V ).
7. Hyperventilation.
8- Removal of K from the body:-
9. K-exchange resins (oral or enema), enhance K clearance across
intestinal mucosa.
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10. Diuretics…40mg I.V furosemide.
11. Dialysis,haemo or peritoneal dialysis.
12- Monitor patient response with:
a- Serum K level
b- ECG.
c- Urine out put
D- The hypokalaemia:- It is defined as serum K level < 3.5 mmol\l.
* Causes of hypokalaemia:
1. Decreased intake (common).
2. Shift into the cells: insulin-glucose administration, alkalosis.
hypothermia.
3. Increased loss: hyper aldosteronism, diuretics, renal tubular
acidosis, vomiting, nasogastric suction, diarrhea, fistula rainage.
* The clinical manifestation of hypokalaemia:
These reflect the diffuse effect of hypokalamaemia on the cell
membranes and excitable tissues.
1- Cardiovascular changes:
a - Dysarrhythmias.
b- ECG changes:
1-Wave appearance.
2. ST-depression.
3. T-wave depression
4. Digitalis toxicity.
2- Neuromuscular changes:
Weakness, Paralysis, Hyporeflexia, Confusion, Depression Constipation,
Ileus.
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* Treatment of hypokalaemia:
1- Correct the precipitating cause like hyper ventilation.
2- I.V or oral KCL:3- In mild hypokalaemia (k-level 2.5-3.5) if the patient cannot tolerate
orally, we can give I.V 10-20mmol kcl to each liter of the fluid.
4- In sever hypokalaemia (k-level < 2.5m.mol\l or paralysis or ECG
changes), it is mandatory to start I.V infusion of kcl at rate of 2040m.mol\h under ECG monitoring, and it requires a central venous
catheter,higher replacement rate may be safest through a femoral
catheter,because very high localized K concentration may occur
within the heart with standard central venous catheter.
5- I.V replacement should not exceed 240meq\day.
6- K-Hco3 or K-acetate or K-citrate is preferable for patient with
metabolic acidosis.
7- K-phosphate is suitable for patient with hypophosphatemia as in
diabetic ketoacidosis.
8- Dextrose containing solutions should be avoided, because the
resulting hyperglycemia and secondary Insulin secretion may
actually lower plasma K.
The available K containing solution:
K-chloride (KCL) ampoules (5ml) containing 10mmol.
It is extremely hyper osmotic and must be diluted before use.
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Head Trauma
HIPPOCRATES: No head injury is so slight that it should be
neglected or so severe that life should be despaired of.
Head injury is one of the commonest sustained injuries presented at
trauma and emergency department.
Head injuries fall into two categories:
a. External injury (usually scalp) and b. internal head injuries, which
may involve the skull, the blood vessels within the skull or the brain.
Traumatic brain injury (TBI) is an important public health problem.
Severe head trauma is a leading cause of death in traumatology today
especially in the young population.
Traumatic brain injuries occurred about 1.5 times as often among
males than females. The majority of TBI cases are children.
A change in the patient s conscious level is the most important
indication of secondary brain damage. The early management from
the scene of injury to the trauma unit with accurate assessment,
thorough resuscitation and definitive treatment are vital to minimize
mortality and morbidity. Most serious head injuries are caused by road
accidents, falls and assaults.
Scalp lacerations are common and could cause severe bleeding if not
early enough controlled.
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I. SKULL FRACTURES.
A. Simple linear skull fracture.
It is a simple fracture line in the skull commonly after blunt trauma
and usually requires no specific neurosurgical management. Such
patients are resuscitated, x-rayed and usually CT scanned and
admitted for close observation for 48 h or more.
Skull fracture left side.
B. Depressed skull fracture.
This type of fracture is a result of blunt trauma where dura and brain
could be lacerated by the depressed fragment. Any damage to the
brain caused at the time of impact with subsequent risk of epilepsy is
irreversible.
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The management includes immediate surgery to prevent infection, to
alleviate mass effect and for cosmetic causes. Surgery is including
debridement of the wound,elevation of the depressed fragment
duraplasty and irrigation before closure with following full course of
intravenous antibiotics.
Depressed skull fracture.
C. Base of skull fracture.
These fractures are relatively frequent and commonly diagnosed on
clinical grounds. They often result in CSF fistula which usually seal
off after a few days.
1. Anterior cranial fossa fractures present with orbital (subconjunctival)
haematomas, anosmia, epistaxis and CSF rhinorrhoea and
occasionally associated with caroticocavernous fistulae and
cranial nerve injuries I to IV.
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