Physiological basis

K+:< ICF: 150 meq/L

       ECF: 3.5 -5 meq/L

• Sodium is the major ECF cation (sodium value 140 mEq/L ECF vs 25 mEg/L intracellular).

Total body k+- 3500meq

• Total body sodium is about 5,000 mEq in a normal adult person.
• 85-90% sodium is extracellular.

K+ -98% Intracellular

       2%. Extracellular

• Sodium is responsible for more than 90% of total osmolality of extracellular fluid.
• Major function of sodium is to maintain ECF volume and therefore maintain blood pressure.
• ECF volume is reflection of total body sodium content (amount).
• Daily requirement of sodium is about 100 mEq or 6 gm of sodium chloride.

K+ requirement is 50-80 meq day

• Excess salt is excreted chiefly by kidney. Loss of sodium in sweat is poor (30-65 mEq/L).]

Response to sodium deficit

• Deficiency of sodium in body will lead to hypovolemia and activates Angiotensin-Il and Aldosterone.
• By acting on the kidney, angiotensin-Il helps to increase sodium absorption at the proximal tubules and aldosterone at the collecting duct.
• In a state of sodium deficit, absorption of Na under aldosterone control is so perfect that almost no urinary Na loss occurs. So by almost complete absorption of Na kidney helps to prevent sodium loss.

Renal priority

• To reclaim sodium under aldosterone influence, initially potassium and it needed later on Htis lost in the urine.
• Due to body’s priority to reclaim Na > H > K, during abnormal loss of all electrolytes (like in diarrhoea) hypokalemia is the commonest abnormality.

Response to sodium excess

• When there is excess amount (content) of sodium it will lead to increased ECF volume, which will lead to decreased Angiotensin-ll, Aldosterone and increase in ANP.
• Decreased angiotensin-ll and aldosterone level will lead to decreased renal reabsorption of sodium.
• Increased ANP will lead to natriuresis and diuresis.
• Hence net result is increased urinary excretion of sodium. Thus extra sodium will be lost.

HYPERNATREMIA

Hypernatremia is defined as plasma sodium concentration greater than 145 mEg/L. Hypernatremia is a less frequent disorder and indicates either lack of water or primary sodium gain.

HYPERNATREMIA IS USUALLY DUE TO WATER DEFICIT AND NOT SODIUM OVERLOAD.

The thirst mechanism is very effective in preventing hypernatremia. So hypernatremia usually does not occur unless there is non-availability of water, impaired thirst or comatose-confused patient unable to drink water.Therefore, hypernatremia is seen chiefly in very young, very old and very sick or debilitated patients. Pure water deficit leading to hypernatremia is called dehydration.

ETIOLOGY

Common causes of hypernatremia are summarized in Table No. 3.4.

Etiology of hypernatremia

Excess water loss.

A.Insensible loss

     Dermal : Heat exposure, severe burns, severe exercise.

     Respiratory : Patient on mechanical ventilator.

B.Renal loss :

     Diabetes Insipidus (central or nephrogenic)

     Excessive diuretics, uncontrolled DM

C.Gastrointestinal losses

     Osmotic diarrhoea.

Water deficit due to impaired thirst.

• Primary hypodypsia, confused or comatose conditions.

Sodium retention.

• Excessive I.V. hypertonic NaCI or NaHCO3

CLINICAL FEATURES

Clinical features of hypernatremia are primarily neurological and they depend upon the rapidity of onset, its duration and its magnitude.This is the only state in which dry sticky mucous membrane is characteristic and body temperature is generally elevated. Major neurological symptoms include nausea, muscular weakness, altered mental status, neuromuscular irritability, focal neurological deficit and occasionally coma or seizures.

In severe acute hypernatremia brain shrinkage may be substantial,exerting traction on the venous sinuses. It can cause intracerebral and subarachnoid hemorrhage which may produce irreversible neurological deficit or even death. The patient may also complain of polyuria or excessive thirst. The signs and symptoms of volume depletion are often present in patient with history of excessive sweating, diarrhea or osmotic diuresis.

Even though there is equal volume of fluid losses, why the patients with hypertonic dehydration are haemodynamically more stable than the patients with isotonic volume depletion

Pure water loss leads to dehydration with hypernatremia (hypertonic dehydration), whereas proportionate combined loss of water and salt in isotonic volume depletion leads to hypovolemia and has normal serum sodium.

In isotonic volume depletion, fluid loss leads to reduction only in ECF volume (and therefore early reduction in intravascular volume) leading to hypotension and reduction in tissue perfusion. While in dehydration due to pure water depletion there is proportionate reduction in total body water (2/3 from ICF and 1/3 from ECF). As ECF volume depletion land therefore intravascular volume depletion, which is 1/4 of ECF) is much less, clinical features are lesser in pure water depletion

DIAGNOSIS

Complete history and examination may provide the clue for etiology of hypernatremia. Renal and glycaemic status, urinary volume, osmolality and glycosuria and response to vasopressin in diabetes insipidus are useful for etiological diagnosis of hypernatremia

TREATMENT

The therapeutic goals are :

1.To stop ongoing fluid loss by treating the underlying causes.

2.To correct water deficit.

Two important factors to decide treatment plan are

i.ECF volume status and

il.Rate of development of hypernatremia.

The important treatment aspects are

• To diagnose and treat specitic etiology (i.e. treating diabetes insipidus,DM, hypokalemia, hypercalcemia etc. and stopping diarrhoea)
• Fluid deficit : The amount of water required to correct the deficit can be calculated from the following equation.

               Water deficit = Plasma Na-140 × 0.6 x body weight in kg.

                                                140

• In addition to water deficit, ongoing and insensible loss needs to be replaced. Correct the total fluid deficit over 48-72 hours.
• Rate of correction : In acute hypernatremia the water deficit can be replaced relatively rapidly, without increasing the risk of cerebral edema. In acute hypernatremia targeted rate of correction of hypernatremia is 1 mEq/L/hr. Rapid correction of chronic hypernatremia is dangerous. It may lead to neurological problems due to development of cerebral edema. Safe rate of correction is reduction of serum sodium by 1 mEq/every 2 hours or 10 mEq/L over first 24 hours.
• Goal of treatment : The goal is to reduce serum Na concentration to 145 mEg/L.
• Deterioration of neurological symptoms after initial improvement suggests the development of cerebral edema and requires temporary discontinuation of water replacement
• Treatment of hypernatremia is water. The safest route of administration of water is by mouth or via a nasogastric tube.
• Acute hypernatremia is treated vigorously with D-5% infusion.Large and rapid infusion of D-5% will lead to hyperglycemia and osmotic diuresis, which may aggravate hypernatremia. If required,hyperglycemia can be combated with insulin therapy.
• Hypernatremia with ECF volume contraction: If there is severe loss of ECF volume with hypotension and azotemia, isotonic saline is given initially until the ECF volume is restored. Subsequently water deficit can be replaced with water by mouth or I.V. 5%-dextrose or 0.45% NaCI.
• Sodium concentration of 0.9% NaCI (154 mEq/L) is greater than the normal serum sodium (140 mEq/L), but is generally lower than the serum sodium concentration in hypernatremia. So initial therapy with 0.9% Nacl,has an advantage of rapid correction of hypotension and avoiding unnecessary rapid fall of serum sodium.
• Method to calculate change in serum Na for given infusate : Change in serum Na concentration, for the infusion of one litre of appropriately selected I. V. fluid, can be calculated by formula mentioned below

Change in serum sodium concentration =

Infusate Na/L – Serum Na

Total body water (L) + 1

or

Infusate (Na + K)/L – Serum Na

Total body water (L) + 1

(For details of Na concentration of infusate and method to calculate total body water refer treatment of hyponatremia).

• Hypernatremia with increased ECF volume : In these patients hypernatremia is secondary to solute administration. The hypernatremia is acute and can be rapidly corrected. These patients are usually volume overloaded. A loop diuretic is administered along with water to facilitate sodium excretion. In patient with massive overload or renal failure dialysis may be necessary.

HYPONATREMIA

Hyponatremia is defined as plasma sodium less than 135 mEg/LHyponatremia is not uncommon in a hospitalized patient (incidence 1.5 to  2.5%), but is rarely seen in an ambulatory patient (if present, reflects a chronic disease status).

Serum sodium reflects the relative proportion of sodium and water.

Hyponatremia usually means water overload and not sodium deficit.

Hyponatremia can occur with normal, low or even high total body sodium.

So basically hyponatremia can be dilutional ( water excretion lesser than water intake and so needs fluid restriction as the most important treatment) or due to sodium loss (needs sodium and fluid supplementation).

• Hyponatremia usually means water retention

ETIOLOGY

Low serum Na leads to decreased serum osmolality, so true hyponatremia is characterized by hypoosmolality. ECF volume varies in hyponatremic patients, depending upon etiology. So etiology of hyponatremia is classified on basis of these two criteria, osmolality and ECF volume.

Pseudo hyponatremia (increase Lipids, increase Proteins, +increase Carbs)

• Normal osmolality: Hyperlipidaemia, Hyperproteinaemia
• High osmolality:Hyperglycaemia, Mannitol

Hyposmolar hyponatremia (true hyponatremia)

A.Hyponatremia with ECF volume depletion

Patient dehydrated reduction in total body sodium exceeds reduction in total body water)

1.Extra renal loss (Urinary sodium < 15 mEq/L)

Vomiting, diarrhea, peritonitis.

2.Renal loss (Urinary sodium > 20 mEq/L)

Excessive diuretics, salt losing nephropathy, diabetic

ketoacidosis, cerebral salt wasting syndrome.

B. Hyponatremia with hypervolemia, increased CF volume

Patient oedematous- Increase in total body water exceeds

increase in total body sodium)

Urinary sodium < 20 mEq/L : CHF, cirrhosis and nephrotic syndrome.

Urinary sodium > 20 mEq/L : Renal failure

C.Hyponatremia with normal ECF volume

(Patient normovolemic, increased total body water)

• SIADH, post operative pain, hypothyroidism, glucocorticoid deficiency, psychogenic polydypsia, drug induced.

CLINICAL FEATURES

The severity of symptoms depends upon the severity of hyponatremia and the rate at which the plasma sodium concentration is lowered. So acute and severe hyponatremia is symptomatic but chronic and mild hyponatremia is well tolerated. The very young and elderly patients are more symptomatic.

DIAGNOSIS

History and physical examination is often helpful in identifying hypovolemic hyponatremia (diarrhea, vomiting, burns, diuretics etc.)

Three important diagnostic tests are

 1. Plasma Osmolality

Low : True hyponatremia

Normal or elevated : Pseudohyponatremia or renal failure.

2. Urine Osmolality

< 100 mOsm/kg or specific gravity < 1.003, diluted urine suggest primary polydypsia with normal water excretion.

> 100 mOm/kg, other causes of hyponatremia in which water excretion is impaired.

3. Urine Sodium Concentration :

< 15 mEq/L effective volume depletion e.g. diarrhea, vomiting

> 20 mEq/L SIADH (normo volemia) or renal salt wasting (diuretics, renal disease or hypoaldosteronism)

 Hyponatremia is usually associated with low plasma osmolality. But if osmolality is normal or high, rule out pseudohyponatremia

 Normal plasma osmolality i2 275- 290 mOsm/kg.

Plasma= 2× Na +Glucose (mg/dI) + BUN (mg/dI)

Osmolality                     18                        2.8

• Associated hyperkalemia suggests renal insufficiency or adrenal insufficiency with hypoaldosteronism.
• Associated hypokalemia and metabolic alkalosis suggest vomitina or diuretic therapy.
• Diuretics induced hyponatremia is almost always due to thiazide diuretics. (Loop diuretics:Water diuresis > hyponatremia infrequent).

TREATMENT

Treatment of hyponatremia must be individualized considering etiology, rate of development (acute vs. chronic), severity and clinical signs and symptoms.dictum; hyponatremeia which davelops quickly, should be treated fast.Whereas hyponatremia, which develops slowly, should be corrected slowly.

Goal of therapy

1.To raise the plasma sodium concentration at a safe rate.

2.To replace sodium deficit or potassium deficit or both.

3.To correct underlying etiology.

In general hyponatremia is corrected acutely by giving sodium to patients who are volume depleted and by restricting water intake in patients who are normovolemic or oedematous.

Specific treatment

• Removal of the drugs responsible for hyponatremia:
• Thiazide Diuretics, Chlorpropamide or .V. Cyclophosphamide.
• Management of physical stress, (postoperative pain).
• Specific treatment for adrenal insufficiency, hypothyroidism, nephrotic syndrome, CHF, uncontrolled diabetes or ketoacidosis,salt losing nephropathy etc.

1. Hyponatremia with hypovolemia

These patients require fluid and salt supplementation which can be done with I.V, isotonic (0.9%) NaCI (or even oral salt containing water) at rate appropriate for the estimated volume depletion. Intake of simple water or I.V. fluid with low Na (0.45% NaCI, Isolyte-M, 5%-dextrose, etc.) should be restricted until the plasma sodium is within the normal range, because it will aggravate hyponatremia.

Diuretics induced hyponatremia is treated with saline with postassium supplementation (30-40 mEq/L).

2 Hyponatremia with hypervolemia (Oedematous state)

Therapy is difficult in oedematous state since sodium supplementation will worsen fluid overload. Such patients are treated with diuretics, salt restriction, fluid restriction (intake < urine output) and correction of potassium deficit in addition to the etiological treatment.

3.Hyponatremia with euvolemia

Hyponatremia with normal or high ECF volume has impaired water excretion with normal or high total body sodium. In such patients fluid restriction is the most important treatment. Adequate restriction of fluid intake will gradually increase serum sodium concentration.

Basic principles of correction of hyponatremia

Treatment of hyponatremia should balance the risk of hypotonicity due to hyponatremia and the risk of therapy.

• To treat or not to treat :

How rapidly hyponatremia should be corrected is a dilemma, Patients with severe hyponatremia (110-115 mEq/L) are at risk of developing severe and potentially irreversible neurological damage and sometimes even death. On the other hand, too rapid correction of severe hyponatremia can produce central pontine myelinosis or osmotic demyelination syndrome (ODS), which can cause substantial morbidity and mortality.

• When to treat,When not to treat :

A.Patient with seizures or other severe neurological symptoms due to hyponatremia needs prompt treatment. In this setting, risk of untreated hyponatremia and cerebral edema is greater than the potential harm of rapid correction. So rapid correction is indicated in acute (<48 hours) symptomatic or severe (serum Na < 120 mEq/L) hyponatremia.Ön the other hand, chronic (> 48 hrs) and mild hyponatremia, with minimal neurological symptoms are at little risk due to hyponatremia. However, these patients can develop demyelination following rapid correction. So there is no necessity to correct these patients rapidly and they should be treated using slower acting therapy such as fluid restriction. Pay particular attention to premenopausal women, elderly and young children as they are more symptomatic and need early treatment.

Chronic asymptomatic hyponatremia

• The targeted rate of plasma sodium should not be greater than 0.5 to 1.0 mEq/L/hour.
• Raise the plasma sodium by less than 10 to 12 mEq/L on the first day and less than 18 mEq/L over the first two days. As per recent recommendations a targeted rate of correction should not exceed 8 mEq/L on any day of treatment.
• If the rate of correction is faster or rise in serum sodium is > 25 mEq/48 hours or correction is made until normonatremia (serum sodium 140 mEq/L) is achieved there is high risk of central pontine myelinosis.

Acute hyponatremia with severe neurological symptoms

These patients require rapid correction of plasma Na with hypertonic saline. Initial rate of rise of Na concentration should be 1.5-2 mEq/L/hr for the first 3 to 4 hours or until the severe neurological symptoms improve. Besides this initial rapid correction rise in the plasma sodium concentration should not exceed 10-12 mEg in first 24 hours. Patient with seizures also require immediate anticonvulsant drug therapy and adequate ventilation.

How long to treat and when to stop acute correction of hyponatremia

A.Regardless of the initial rate of correction, chosen acute treatment should be interrupted once any of the three end points is reached

1) Patient’s symptoms are abolished.

2) A safe plasma sodium (generally 120-125 mEq/L) is achieved or

3.A total magnitude of correction of 20 mEq/L is achieved. It is necessary to correct hyponatremia accurately to a safer range,rather than correcting completely to normonatremia.

Fluid should be used to correct hyponatremia

• Aim of fluid infusion is to raise Na. by correcting Na delicit, so the infused fluid should contain higher Na concentration than desired or normal serum sodium concentration.
• 0 9% saline (154 mEQ/L Na) and 3% NaCl-hypertonic saline (513mEq/L Na) are the only two routinely used IV fluids which have higher Na concentration and therefore are used to correct hyponatremia. However, for the treatment of hyponatremia due to SIADH, infusion of 0.9% NaCI is inappropriate.
• When hyponatremia is associated with hypovolemia or in absence of fluid retention or edema, 0.9% saline is the preferred fluid.
• But when patient needs salt supplementation along with fluid restriction hypertonic saline is the preferred fluid (e.g. severe form of SIADH).

Monitor Na during treatment of hyponatremia

During treatment of hyponatremia, many other independent factors can modify the Na concentration (e.g. urinary and other losses of Na, addition of oral fluid intake etc.). So frequent monitoring of the serum sodium concentration (atleast at 4 to 6 hours interval initially), is necessary to ensure that the rate of correction is as desired and in order to make further adjustment in the amount and rate of fluid administration. Remember, in symptomatic/sick patients with hyponatremia, calculation of the requirement of Na containing IV. fluids for whole 24 hours and their infusion without proper monitoring and modification can be dangerous.

Condition in which appendix become inflamed.

HOW TO IDENTIFY CLINICALLY

• Pain- Migratory pain (initial around umbilicus later in the right iliac foss)
• Vomiting
• Fever

CHARACTERESTIC FEATURES/ DIAGNOSTIC FEATURS

• Abdominal pain
• Swollen belly
• Constipation
• Diarrhea
• Inability to pass gas
• Loss of appetite
• Low grade fever
• Nausea and vomiting
• Tenderness & reborn tenderness in right iliac fossa.

LAB DIAGNOSIS

Gold test- contrastenhance computed tomography(CECT)

Initial test- abdominal X-ray, abdominal ultrasound,  MRI,  CT-scan, urine test,  blood test

WARNING SIGNS

• Peritonitis
• Abdominal guarding
• Painful abdomen
• Distended tenderness
• Reboud
• Absent bowl sound

INITIAL MANAGEMENT

• Nill by mouth
• Insertion of Rule’s tube if vomiting
• I.V. Fluids
• I.V. antibiotics- ofloxacin + metrogyl

DEFINITIVE MANAGEMENT

• If no appendicular mass-

SURGERY

• Laparoscopic appendectomy/ open appendectomy.

• If appendicular mass-

• Conservative management (NMB, IV Fluids,IV antibiotics)
• Following interval appendectomy after 6 months.

Infection resulted in muscles due to intramuscular injection

Clinical identification:

• History of injection to the site
• Swelling at the site of injection
• Redness at the site of injection
• Fever
• Difficulty in moving the limb

Characterstics features:

• Along with above symptoms Tenderness may be present
• Fluctuations may be present in some cases

Lab diagnosis:

• Gold standard: High resolution ultrasonography
• Initial tests: CBP- Elevated WBC count

Warning signs:

• Persistent pain and fever
• Signs of sepsis
• Positive fluctuation test

PEM’S initial management:

• Local care
• Cold compress
• Antibiotics :

              AUGMENTIN 625mg TID

              CLINDAMYCIN 300mg TID

• Analgesics/ Anti inflammatory
• IV formulation in Diabetics and Immunocompromised patients

Definitive management

• Drainage of abscess, wound care
• Sensitivity based Antibiotics

Submitted by

P.Bharathi

• In diarrhoea stool contains large amount of sodium chloride,potassium,bicarbonate along with water.

ELECTROLYTE CONTENT OF DIARRHOEA : [mEq/L]

FLUID &ELECTROLYTE ABNORMALITY IN DIARRHOEA IS SUMMARIZED BELOW: 

1. HYPOVOLEMIA :
2. Abnormal increased secretion of fluid into the small bowel [secretory diarrhoea due to GI infection e.g-E.coli,Vibrio Cholerae,Rota virus]
3.  Decreased absorption of fluid by intestine [osmotic diarrhoea due to purgatives like magnessium sulphate/malabsorption of glucose/lactate in children.
4. Additional loss of water can also occur due to associated vomiting/fever.
5. SODIUM DEFICIT :
6. Diarrhoea cause loss of  sodium,resulting in sodium deficit in all patients,but proportion of sodium loss as compared to water loss will decide serum sodium concentration and type of dehydration
7. In some infants with diarrhoea net loss of water is in excess of sodium which leads to hypertonic dehydration
8. If net loss of sodium is greater than loss of water,diarrhoea will cause hypotonic dehydration
9. HYPOKALEMIA :
10. Hypokalemia occurs because fluid lost in diarrhoea is rich in potassium.
11. Normally 8-15mEq potassium ions are excreted in             faeces daily.much greater loss occurs with diarrhoea
12. HYPERCHLOREMIA :
13. The ileal and colonic mucosa possesses a luminal chloride/bicarbonate exchanger that is capable of reabsorbing chloride in exchange of bicarbonate
14. So during diarrhoea when more bicarbonte is secreted,more chloride is absorbed from intestine causing hyperchloremia.
15. METABOLIC ACIDOSIS :
16. fluid secreted distal to pylorus is rich in bicarbonate.
17. Diarrhoea leads to large amount of bicarbonate secretion [30-45mEq/L] in the gut which is excreted,and leads to metabolic acidosis.
18. If diarrhoea causes severe hypovolemia or renal failure,renal compensation to loss of bicarbonate is lost and severe metabolic acidosis may develop rapidly.
19. Acidosis may also result from excessive production of lactic acid when patient has hypovolemic shock.
20. So hyperchloremic,hypokalemic,metabolic acidosis occurs in patients with diarrhoea.

TREATMENT :

• Specific treatment for control of diarrhoea
• Fluid therapy

AIM OF FLUID THERAPY IS :

• Correction of dehydration
• Correction of sodium deficit
• Correction of hypokalemia & metabolic acidosis.treatment of both need to be done simultaneously. If only metabolic acidosis is treated,due to its correction potassium will be shifted intracellularly. If patient is hypokalemic,only correction of the acidosis can precipitated dangerous hypokalemia

                         On the contrary,with out correction of acidosis, potassium supplementation can cause dangerous hyperkalemia.this is due to failure of potassium shift into the intracellular compartment even in state of potassium deficit of the body. 

• Fluid and electrolytes losses can be replaced either orally/intravenously.intravenous route is usually needed only for initial rehydration of patients with severe diarrhoea.
• ORAL REHYDRATION THERAPY :
• Oral rehydration therapy is easily available,simple to use and safe.
• It is preferred method of fluid replacement.losses due to diarrhoea can be effectively corrected by oral rehydration solutions[ORS].
• Readily available ORS provides sodium,potassium,chloride and bicarbonate along with glucose,which effectively corrects fluid and electrolyte abnormalities,and also provide calories.
• Glucose enhances sodium and secondary water transport across the mucosa of the upper intestine,even in presence of infective diarrhoea.
• Avoid correction of losses due to diarrhoea,totally with electrolyte free solutions.as it provides only fluid,but lacks electrolytes,it can cause hyponatremia and is not effective in correction of hypovolemia.
• INTRAVENOUS FLUID THERAPY :
• I.V fluid therapy is indicated when rapid correction of blood volume is required for severe dehydration and shock,inability of patient to take ORS due to persistent vomiting or ORT fails to correct volume depletion due to greater losses.
• The preferred I.V fluids to correct losses due to diarrhoea are ringers lactate and isotonic saline.
• RINGERS LACTATE SOLUTION :
• It is the best commercially available solution
• It is the preffered solution because it not only provides an adequate concentration of sodium but also provides bicarbonates for the correction of metabolic acidosis
• Its potassium & solution provides no glucose to prevent hypoglycemia.so the patient with diarrhoea may require additional potassium,glucose,and at times bicarbonate supplementation.
• ISOTONIC SALINE:
• It effectively corrects hypovolemia and provides sodium along with water. Isotonic saline does not contain potassium to replace potassium deficity or base to correct metabolic acidosis.
• So patient may require additional supplementtion of potassium[10-20mEq/L]and sodium bicarbonate [20-30mEq/L] to correct existing hypokalemia and metabolic acidosis.
• 5% DEXTROSE ;
• It is not an acceptable I.V fluid because it does not correct acidosis,hypokalemia,and sodium deficity
• 5% dextrose is not effective in correction of hypovolemia .
• Rapid infusion large volume of 5% dextrose also carries the risk of hyponatremia and hyperglycemia leading to osmotic diuresis
• However,dextrose 5%with 45mEq bicarbonate [2 amp-50ml of 7.5% of sodium bicarbonate] and 20-30mEq of potassium chloride is effective

TRIMODAL PEAK OF DEATH:

1st Peak ( Immediate ) 50%

• Within first few minutes of injury
• Extensive trauma to Brain, Upper Spinal Cord, Heart or Major Blood Vessels, Rupture of Major Airway.
• Little can be done to salvage the Patient.

2nd Peak ( Early Deaths ) 30%

• Within first few hours of Injury
• Subdural/Epidural Hematoma
• Hemo/Pnemothorax
• Organ Rupture/Blood Loss
• Pelvic/long Bone Fracture

3rd Peak ( Late Deaths) 20%

• Weeks after Injury
• Multiorgan failure
• Sepsis

MANAGEMENT OF POLY-TRAUMATIZED PATIENT

There are many protocols for management of poly-trauma, the most universally accepted one is the protocol of ATLS (ADVANCED TRAUMA LIFE SUPPORT) which described by the American College of Surgeons, which consists of 3 steps:

• Primary survey.
• Secondary survey.
• Definitive treatment.

Another protocol is the 5 Rs, as follows

• R1: Rapid Evaluation = Triage.
• R2: Resuscitation.
• R3: Radiology and Other Investigations.
• R4: Re-Evaluation.
• R5: Repair and Rehabilitation.

 R1: RAPID EVALUATION = TRIAGE

Within few seconds you have to be able to put your patients in one of the following categories;

• Black (White) Zone: for those who are dead or dying(e.g. brain herniation).

• Red Zone: for those who needs urgent interference within 5-10 minutes (e.g. those with external hemorrhage and respiratory compromise).

• Yellow Zone: for those who needs also urgent intervention but could withstand for 1-2 hours with in which some resuscitation and investigations could be done (e.g. Internal hemorrhage patients).

• Green Zone: for those who needs intervention within 1-2 days (e.g. patients with fractures).

R2: RESUSCITATION

Including the urgent measures that should be done for the patient immediately after the accident (in the field of the accident) to save his life during the first minutes or hours(the golden hours), they should be done in the order of priority A B C D E as follows:

A-Airway:

B-Breathing:

C-Circulation:

D-Disability (Neurological Assessment):

E-Exposure:

A-AIRWAY:

• The patient’s airway should be evaluated and protected. In general, if the patient is capable of unstrained speech, his airway is patent. All patients should receive supplemental oxygen by mask till they reach the hospital.

Asses for: obstruction, facial fractures, tracheal injuries, tracheal deviation.

• Apply hard cervical collar.
• Open airway by doing jaw thrust maneuver (chin lift).
• Open the mouth, remove the obstruction or secretion. Do suction to remove any obstruction (e.g. secretions, blood, vomitus or any foreign body).

Insert oro-pharyngeal or naso-pharyngeal airway to maintain patency of airway and to prevent falling back of the tongue in an unconscious patient. This method is contra-indicated in conscious patients (stimulates gag reflex and vomiting)

Endo-tracheal Intubation (indicated in cases of apnea, head injuries, air way compromise like maxillofacial injuries, fracture cervical spine and if there is risk of aspiration).

Cricothyroidotomy : If there is upper airway obstruction and it is impossible to pass an endo-tracheal tube.

B-BREATHING:

Check for spontaneous breathing for 10 sec;

• If patient is breathing satisfactorily & PO2 above 90%» justobserve.
• If patient is breathing satisfactorily but PO2 below 90% »provide o2 therapy via mask 6 L/min, 60% O2 concentration.
• If patient is not breathing or PO2 still declining » manually ventilate patient with 15L/min, 100% oxygen concentration &Prepare for intubation and mechanical ventilation.

C-CIRCULATION:

Check peripheral pulsations: tachy- or brady- cardia.

Check Blood Pressure: be rapid and accurate in its measurement.

Check neck veins: is it

• Collapsed—– Hypovolemia.
• Distended—- Impaired Venous Return.
• Tension Pneumothorax; treat it immediately.
• Cardiac Tamponade; treat it immediately by Pericardiocentesis
• Myocardial Contusion & Infarction.

Fluids:

• 2 large bore IV Cannulas&starting with bolus IV fluids-10ml/kg(crystalloid)usual choice RL&NS
• If patient is stable maintenance fluids according to  patients weight will be continued &monitored with the help of blood pressure& urine output
• If immediate blood is not available patient can be started on crystalliods(HEMECEAL)after taking sample for blood group testing.
• O-ve can be transfused without waiting for grouping if available.

If the patient is in shock (neurogenic, oligaemic or cardiogenic), start

immediately anti-shock measures (arrest of bleeding, infusion of lactated

Ringer’s sol., and blood transfusion once available).

D-DISABILITY (Neurological Assessment):

Level of consciousness.

• AVPU scale;

• Awake.
• Verbal response.
• Pain response.
• Unresponsive.

For assessment, apply any scale e.g Glasgow Coma Scale.

GLASGOW COMA SCALE

• 3 – 15 point scale to assess mental status only
• Best observed response
• GCS ≤ 8 is a “coma” and requires intubation for airway protection

E-EXPOSURE:

• Remove clothing.
• Observe the chest for bruises, penetrations, and symmetry.
• Auscultate breath sounds.
• Auscultate heart sounds.
• For total assessment.

After exposure you may find:

Ecchymosis at site of trauma.

R3: RADIOLOGY & OTHER INVESTIGATIONS.

I- Basic X-Ray Films have to be done for every case of Polytrauma depends largely on the suspected site and the doctor who is going to request it. Every specialty has its own interest;

General Surgery: erect abdomen

Cardiothoracic Surgery: chest x-ray

Neurosurgery: skull and spines

Orthopedic Surgery: pelvis, spine and fractures

R4: RE-EVALUATION

(Secondary survey)

Now, this is the time of re-evaluation of the patient. It is done in two steps:

-History taking: this includes; SAMPLE;

• Symptoms.
• Allergies.
• Medications.
• Past history.
• q2Last meal.
• Events related to injury.

II-General Examination from Hair to Heal:

1.Head: search for sub-galeal hematoma, sub-conjunctival hemorrhage, facial fractures,…etc.

2.Neck: pain or tenderness, tracheal deviation, jugular vein, impaled objects and open wounds, Expanding neck hematoma.

3.Heart: rib fractures, pneumo- or hemo-thorax,…etc.

4. Abdomen & Pelvis: Cullen’s sign, Grey-Turner sign,Kher’s sign,…etc.

5.Extremities: Fractures, peripheral pulsations, soft tissue injuries,…etc.

6.Back: bruising, impaled objects, pain and tenderness.

Chest:

   Inspect the chest, observe the chest movements. Look in

particular for:  

• bruising (from seat-belts)
• asymmetric or paradoxical chest wall movement
• penetrating wounds are rare in children, but in cases

where there is a stabbing or other assault look for

“hidden” wounds – checking areas such as the axilla and

back

Palpate for clavicular and rib tenderness and auscultate the

lung fields and heart sounds.

Abdomen:

Inspect the abdomen, the perineum and external genitalia. Look

for in particular for:

   seat-belt bruising / handle-bar injuries

• distension

• blood at the urinary meatus / introitus

Palpate for areas of tenderness especially over the liver, spleen,kidneys and bladder, and auscultate bowel sounds.

Pelvis:

Inspect the pelvis for grazes over the iliac crest. Examine for bruising, deformity, pain or crepitus on movement.

R5: REPAIR & REHABILITATION.

(Definitive treatment of individual injuries )

Finally, the patient is admitted to the hospital in one of the following destination sites:

• General Surgery Department.
• Neurosurgery Department.
• Orthopedic Surgery Department.
• Cardiothoracic Surgery Department.
• ICU.