• Typhoid fever is the result of systemic infection mainly by salmonella typhi found in only humans.
• The disease is clinically characterized by a typical continuous fever for 3 to 4 weeks, relative bradicardia with involvement of lymphoid tissues and considerable constitutional symptoms.
• The term “enteric fever” includes both typhoid ad paratyphoid fevers.
• Typhoid fever is endemic in India.
• Reported data for the year 2013 shows 1.53 million cases and 361 deaths.
• The factors which influence the onset of typhoid fever in man are the infecting dose and virulence of the organism.
• Man is the only known reservoir of infection, viz., cases and carriers.
• The primary source of infection are faeces and urine of cases or carriers, the secondary sources are contaminated water, food, fingers and flies.
• There is no evidence that typhoid bacilli are excreted in sputum or milk.

CAUSES:

• Typhoid fever is contracted by drinking or eating the bacteria in contaminated food or water.
• People with acute illness can contaminate the surrounding water supply through stool, which contains a high concentration of the bacteria.
• About 3%-5% of people become carriers of the bacteria after the acute illness. Others suffer a very mild illness that goes unrecognized.
• These people may become long-term carriers of the bacteria even though they have no symptoms and be the source of new outbreaks of typhoid fever for many years.

SIGNS AND SYMPTOMS:

• High fever
• Diarrhea
• Rose spots
• Aches and pains
• Poor appetite
• Lethargy

MODE OF SPREAD:

• Typhoid fever is transmitted via the faecal- oral route or urine- oral route.
• This may take place directly through soiled hands contaminated with faeces or urine of cases or carriers, or indirectly by the ingestion of contaminated water, milk and/or food or through flies.

INCUBATION PERIOD:

• Usually 10-14 days. But it may be as short as 3 days or as long as 3 weeksdepending upon the dose of the bacilli ingested.

CLINICAL FEATURES:

• FIRST WEEK: malaise, headache, cough and sore throat in prodromal stage. The disease classically presents with step- ladder fashion rise in temperature over 4 to 5 days., accompanied by headache, vague abdominal pain and constipation or pea soup diarrhea.
• SECOND WEEK: between the 7 – 10 days of illness, mild hepatoslenomegaly occurs in majority of the patients. Relative bradycardia may occur and rose spots may be seen.
• THIRD WEEK: the patient will appear in the typhoid state, which is a state of prolonged apaty, toxemia, delirium, disorientation and/or coma. Diarrhea will then become apparent. If left untreated by this time, there is a risk( 5-10%) of intestinal hemorrhage and perforation.

PATHOPHYSIOLOGY:

Ingestion of contaminated food/ water

Carried by white blood cells in the liver, spleen and bone marrow

Multiply and reenter the bloodstream

Bacteria invade the gallbladder, biliary system and the lymphatic tissue of the bowel and multiply in higher number.

Then pass into the intestinal tract and can be identified for diagnosis in cultures from the stool tested in the laboratory.

LAB INVESTIGATIONS:

• Blood culture.
• Specific serologic test:
  • Identify salmonella antibodies/ antigens
  • Widal test and ELISA.
• Urine and stool culture.
• Marrow culture*: 90% sensitive unless until after the commencement of the antibiotics.
• Punch – biopsy samples of rose spots culture: 63% sensitive.
• Clot culture.

TREATMENT:

• SUPPORTIVE CARE:   –    maintenance of adequate hydration.

–    Appropriate nutrition

• SPECIFIC CARE:          –     Antibiotics
• Corticosteroids
• Antipyretics
• ANTIBIOTICS like chloramphenicol(200mg,QID), ampicillin(750mg, QID), Co- trimaxazole( 2 tablets/ IV BDS), fluroquinolones like ciprofloxacin(500mg BDS).
• Incase of quinolone resistance – Azithromycin(500mg/ OD) and third generation cephalosporins like ceftriaxone( alternative).
• The treatment should be continued for 14 days.

PREVENTION:

• Regular hand wash.
• Drinking boiled water.
• Cleaning fruits and vegetables before their use.
• Get vaccinated.

RED FLAGS:

                      Sudden onset severe abdominal pain with garding and rigidity.

PITFALLS:

                      Other infection peptic ulcer with perforation.

PEARLS:

                     To avoid outside food intake &contaminated food intake.

REFERENCES:

• https://www.slideshare.net/yuyuricci/enteric-fever-typhoid-fever.
• www. webmd. com .

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.

Limb ischemia is a severe blockage in the arteries of the lower extremities, which significantly reduces blood flow. Acute limb ischemia is a sudden and rapid decrease in lower limb blood flow. 

TYPES

• Acute limb ischmia
• Chronic limb ischemia
• Critical limb ischemia

Acute limb ischemia

• Acute limb ischemia is a sudden and rapid decrease in lower limb blood flow. 

Chronic limb ischemia

• Chronic limb ischaemia is peripheral arterial disease that results in a symptomatic reduced blood supply to the limbs.
• It is typically caused by atherosclerosis (rarely vasculitis) and will commonly affect the lower limbs (however the upper limbs and gluteals can also be affected)
• Chronic limb ischaemia is a common condition, ranging in severity across the population, associated with several cardiovascular risk factors
• Whilst a clinical diagnosis, it can be quantified by ABPI testing, following by angiogram imaging
• Surgical intervention can be offered if conservative management options fail or those presenting with critical limb ischaemia.

Critical limb ischemia

Critical limb ischaemia is the advanced form of chronic limb ischaemia.

It can be clinically defined in three ways:

• Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
• Presence of ischaemic lesions or gangrene objectively attributable to the arterial occlusive disease.
• ABPI less than 0.5

There are three main stages of acute limb ischemia: 

• Stage 1: Viable
  • Limb is not immediately threatened
  • No sensory loss
  • No muscle weakness
  • Doppler signals of arteries and veins are audible
• Stage 2: Threatened 
  • Stage 2a: Marginally threatened 
    • Limb is salvageable if promptly treated
    • Minimal sensory loss (toes) or no sensory loss
    • No muscle weakness
    • Doppler signals of arteries are often inaudible; veins are audible
  • Stage 2b: Immediately threatened 
    • Limb is salvageable with immediate revascularization
    • Sensory loss is more than toes, associated with rest pain
    • Mild to moderate muscle weakness
    • Doppler signals of arteries are usually inaudible; veins are audible
• Stage 3: Irreversible 
  • Limb has major tissue loss or permanent nerve damage inevitable
  • Profound sensory loss, numbness
  • Profound weakness, paralysis 
  • Doppler signals of arteries and veins are inaudible

EPIDEMOLOGY

The major cause of acute limb ischaemia is arterial embolism (80%), while arterial thrombosis is responsible for 20% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a blood clot or embolism resulting in ischaemia.

ETIOLOGY

Causes of acute limb ischemia include: 

• Blockage in a blood vessel (embolism) by such as by a blood clot, a fat globule, a bubble of air or other gas, or foreign material
• Blood clot (thrombosis)
• Peripheral artery disease due to atherosclerosis
• Tear in the lining of an aortic or peripheral artery (dissection)
• Major trauma
• Conditions that cause vasospasm 
  • Raynaud phenomenon
  • Shock (e.g., meningococcal sepsis, cardiogenic shock)
  • Administration of vasoactive drugs

Most acute limb ischemia is caused by embolism, thrombosis, peripheral artery disease due to atherosclerosis, or major trauma.

SYMPTOMS

Acute limb ischaemia can occur in patients through all age groups. People who smoke tobacco cigarettes and have diabetes mellitus are at a higher risk of developing acute limb ischaemia.Most cases involve people with atherosclerosis problems.

Symptoms of acute limb ischaemia include:

• Pain
• Pallor (pale appearance of the limb)
• Paresthesias (abnormal sensations in the limb)
• Pulselessness
• Paralysis

DIAGNOSIS

Acute limb ischemia diagnosed with a patient history and physical examination. The blockages associated with limb ischemia are located using one or more of the following methods:

• Auscultation
• Ankle-brachial index (ABI)
• Doppler ultrasound 
• Computerized tomography (CT) angiography
• Magnetic resonance angiography (MR angiography)
• Invasive Angiogram

ALI is diagnosed on the basis of medical history, visual examination, palpation, and Doppler examination of the peripheral arterial pulse using vascular ultrasonography and contrast-enhanced computed tomography (CT) as imaging tests

Investigation –

Suspected cases should be initially investigated with beside Doppler ultrasound scan (both limbs), followed by considering a CT angiography.

If the limb is considered to be recoverable, a CT arteriogram can provide more information regarding the anatomical location of the occlusion and can help decide the operative approach

• In order to treat acute limb ischaemia there are a series of things that can be done to determine where the occlusion is located, the severity, and what the cause was.
• To find out where the occlusion is located one of the things that can be done is simply a pulse examination to see where the heart rate can be detected and where it stops being sensed. Also, there is a lower body temperature below the occlusion as well as paleness.
• A Doppler evaluation is used to show the extent and severity of the ischaemia by showing flow in smaller arteries.
• Other diagnostical tools are duplex ultrasonography, computed tomography angiography (CTA), and magnetic resonance angiography (MRA).
• The CTA and MRA are used most often because the duplex ultrasonography although non-invasive is not precise in planning revascularization. CTA uses radiation and may not pick up on vessels for revascularization that are distal to the occlusion, but it is much quicker than MRA.^[1] In treating acute limb ischaemia time is everything.
• In the worst cases, acute limb ischaemia progresses to critical limb ischaemia, and results in death or limb loss.
•  Early detection and steps towards fixing the problem with limb-sparing techniques can salvage the limb.
• Compartment syndrome can occur because of acute limb ischaemia because of the biotoxins that accumulate distal to the occlusion resulting in edema.

Immediate treatment is needed for limb ischemia to re-establish blood flow to the affected area and to preserve the limb.

TREATMENT

Treatments for acute limb ischemia include: 

• Intravenous (IV) injection of unfractionated heparin (15–20 units/kg)

Upon the diagnosis of ALI, as long as heparin therapy is not contraindicated,an intravenous injection of unfractionated heparin (50–100 units/kg) is immediately administered to prevent the proximal and distal progression of secondary thrombosis to the site of occlusion, and a systemic administration of thrombolytic agents is not recommended. 

• Surgical treatment 
  • Thromboembolectomy
  • Bypass surgery
• Endovascular treatment 
  • Catheter-directed thrombolysis (CDT)
  • Percutaneous thrombus aspiration
  • Stent placement

extensive ischemia due to high occlusion and when time has passed since its onset, there is a high risk of severe ischemia–reperfusion injury; thus, limb amputation might be necessary to prioritize the patient’s life.

• Hybrid treatment that combines both therapies

Hybrid interventions in vascular surgery are defined as the utilization of both open surgical and endovascular techniques simultaneously in a single setting operation.

Red flags

missing stage 2 presentation

Pit falls –

window period causing peripheral limb loss

Pearls –

prompt mangement in stage -1 will save patient limb

• Daibetic control
• Frequent monitoring of limb

• Low back pain can result from many different injuries, conditions or diseases — most often, an injury to muscles or tendons in the back.
• Pain can range from mild to severe.
• In some cases, pain can make it difficult or impossible to walk, sleep, work or do everyday activities.
• Usually, lower back pain gets better with rest, pain relievers and physical therapy (PT).
• Some back injuries and conditions require surgical repair.

RISK FACTORS:

• Age: People over 30 have more back pain. Disks (soft, rubbery tissue that cushions the bones in the spine) wear away with age. As the disks weaken and wear down, pain and stiffness can result.
• Weight: People who are obese or carry extra weight are more likely to have back pain. Excess weight puts pressure on joints and disks.
• Overall health: Weakened abdominal muscles can’t support the spine, which can lead to back strains and sprains. People who smoke, drink alcohol excessively or live a sedentary lifestyle have a higher risk of back pain.
• Occupation and lifestyle: Jobs and activities that require heavy lifting or bending can increase the risk of a back injury.
• Structural problems: Severe back pain can result from conditions, such as scoliosis, that change spine alignment.
• Disease: People who have a family history of osteoarthritis, certain types of cancer and other disease have a higher risk of low back pain.
• Mental health: Back pain can result from depression and anxiety.

SYMPTOMS:

• Symptoms of lower back pain can come on suddenly or appear gradually.
• Pain may be sharp or dull and achy, and it may radiate to your bottom or down the back of your legs.
• If you strain your back during an activity, you may hear a “pop” when it happened.
• Pain is often worse in certain positions (like bending over) and gets better when you lie down.
• Other symptoms of lower back pain include:
  • Stiffness
  • Posture problems
  • Muscle spasms.

CAUSES:

• Strains and sprains
• Fractures
• Disk problems
• Structural problems
• Arthritis
• Infections and tumors
• Spondilolisthesis

DIAGNOSIS:

• Spine X-ray
• MRI
• CT scan

TREATMENT:

• Lower back pain usually gets better with rest, ice and over-the-counter pain relievers. After a few days of rest, you can start to get back to your normal activities. Staying active increases blood flow to the area and helps you heal.
• Other treatments for lower back pain depend on the cause. They include:
• Medications: Your provider may recommend nonsteroidal anti-inflammatory drugs (NSAIDs) or prescription drugs to relieve pain. Other medications relax muscles and prevent back spasms.
• Physical therapy (PT): PT can strengthen muscles so they can support your spine. PT also improves flexibility and helps you avoid another injury.
• Hands-on manipulation: Several “hands-on” treatments can relax tight muscles, reduce pain and improve posture and alignment. Depending on the cause of pain, you may need osteopathic manipulation or chiropractic adjustments. Massage therapy can also help with back pain relief and restore function.
• Injections: Your provider uses a needle to inject medication into the area that’s causing pain. Steroid injections relieve pain and reduce inflammation.
• Surgery: Some injuries and conditions need surgical repair. There are several types of surgery for low back pain, including many minimally invasive techniques

PREVENTION:

• You can’t prevent lower back pain that results from disease or structural problems in the spine.
• To reduce your risk of a back injury, you should:
• Maintain healthy body weight
• Strengthen your abdominal muscle

• Lift in a right way.

RED FLAGS :

• Weakness of upper limb/lowerlimb
• Numbness
• Bowel or bladder disturbances
• Radiating pain to upper limb/lower limb

Their symptoms may need surgical intervention after evaluation

Objects in the mouth may be swallowed or breathed (aspirated) into the lungs

Objects in the ears and nose can make it hard to hear or breathe and can cause infection

FOREIGN BODIES IN THE EAR:

Foreign bodies in the ear canal be anything a child can push into his or her ear

Some of the items that are commonly found in the ear canal include

Food

Insects

Toys

Buttons

Pieces of crayon

Small batteries

« Some objects placed in the ear may not cause symptoms

« Other objects such as food and insects may cause pain in the air,redness or drainage

« Hearing may be affected if the object is blocking the ear canal

Techniques that may be used to remove the object from the ear canal:

Instruments such as long, thin tweezers or forceps may be put in the ear to grab and remove object

Magnets are sometimes used to remove the object if it is metal

The ear canal may be flushed with water

A machine with suction may be used to help pull the object out

After removal of the object, re-examine the ear to determine if there has been any injury to the ear canal

Antibiotic drops for the ear prescribed to treat any possible outer ear infections

FOREIGN BODIES IN THE NOSE:

Objects that are put into the childs nose are usually soft things

These include

Ÿ Tissue

Ÿ Clay

Ÿ Pieces of toys

Ÿ Erasers

« The most common symptom of a foreign body in the nose is nasal drainage

« Often has a bad odour

« In some cases, the child may also have a bloody nose

Techniques :

Sedating the child is sometimes needed to remove the object successfully

Suction machines with tubes attached may be used

Instruments may be inserted in the nose

The object may be blown out of the nose

After removal of the object, prescribe nose drops or Antibiotic ointment to treat any possible infections

FOREIGN BODIES IN THE THROAT :

A foreign body in the throat can cause choking and is a medical emergency that needs immediate attention. The foreign body can get stuck in many different places within the Airway.

According to the American Academy of Pediatrics death by choking  is leading cause of death and injury among children younger than 4 yrs of age

Ÿ Seeds                         

Ÿ Toy parts

Ÿ Grapes

Ÿ Hot dogs

Ÿ Pebbels

Ÿ Nuts

Ÿ Buttons

Ÿ Coins

Symptoms that may mean a child is choking

« Choking or gagging when the object is first inhaled

« Coughing at first

« Wheezing (A whistling sound usually made when the child breaths out)

 Symptoms may mean that the foreign body is still blocking an airway

« Stridor ( A high pitched sound usually heard when the child breathes)

« Cough that gets worse

« Child unable to speak

« Pain in the throat area or chest

« Hoarse voice

« Blueness around the lips

« Not breathing

« The child becoming unconscious

If the FB is visualised in the oropharynx and the patient can tolerate the procedure, removal may be attempted using Magill forceps. Otherwise, removal should be attempted with endoscopy under GA (either via pharyngoscopy / laryngoscopy or rigid oesophagoscopy).

The urgency of endoscopy is outlined below:

• Emergency endoscopy
  • Any red flag signs
  • Any sharp or long (>5cm) object in the oesophagus
• Urgent endoscopy (within 24 hours)
  • Oesophageal obstruction (unable to swallow saliva)
  • Blunt oesophageal FB
  • Magnets proximal to the duodenum
• Non-urgent endoscopy
  • Disc or cylindrical batteries which have passed into stomach without signs injury
  • coins may be observed for upto 24 hours before removal if asymptomatic

To prevent choking:

Cut foods into small pieces

Never let small children run, play or lie down while eating

Keep coins and small items out of reach of your children

Read warning labels on toys

Learn first aid for choking

Submitted by

P.Bharathi

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

•    It is viral infection of nose & throat.

•    The term common cold refer as mild upper respiratory viral illness.

•    Usually lasts approximately for 7 days.

•    Cold caused by many viruses which is having similar symptoms. (Eg. Rhinovirus, coronavirus, adenovirus, echovirus, enterovirus)

TRANSMISSION

•    Direct contact- primary spread from person to person person to person through hands. If sick person shake someone’s hand and that percentage is eye, nose or mouth, the viras can           transmitted & later infect.

•    Indirect- virus can survive on surface  for few hours can transmitted touching the surface and then touching his nose, mouth or eyes.

•    Inhaled viral particles- droplet containing viral particle can be transmitted while coughing, sneezing, breathing to close standing person.

CLINICAL FEATURES

•    Rhinitis (runny nose)

•    Sore throat

•    Sneezing

•    Cough

•    Headache

•    Fever seen in children, uncommon in adults.

•    Feeling tired.

INCUBATION PERIOD (24-72 hrs)

Symptoms usually 3- 10 days, last upto 2 weeks in some peoples

DIAGNOSIS

  The diagnosis is based on symptoms and observed signs:-

•    Swelling and congestion of nasal passages

•    Redness of the throat

•    Enlarged lymph nodes in the neck

•    Normal lung exam

Chest x-rays not needed unless chest exam is abnormal

LAB TEST

generally not needed

•    Detection of antigen (rapid test)

•    Viral isolation

•    Serology

COMPLICATIONS

•    exacerbation of  Asthma, COPD.

•    Acute bacteria bronchitis

•    Pneumonia

•    Strep throat (sore & scratchy throat)

•    Acute ear infections

TREATMENT Symptomatic

•    Antihistamine – for runny nose, sneezing, cough.

• diphenhydramine (benadryl) –  300mg/QID
• levocitrizine- 10mg/day – OD
• Chlor pheneramine – 24mg/ day – TID

•    Antitussive– for dry cough.

• Codeine- 10mg/5ml – TID ODextra methorphan – 30mg/5ml – TID

•    Expectorant– for productive cough.

•  Guaifenesis- 2.4g/day – TID
•  Acetyl cystein- 5- 10ml of 10-20% of solution 6-8 hr if needed.
•  Bromhexin- 400mg/5ml – TID

•    Docongestants– for block nose. OEphedrine-5-25mg iv

•  Phenyl ephedrine- 200mcg
•  Oxymethazoline 0.05% 2-3 sprey

•    Analgesic– for headache, sore throat, muscle ache, fever, chillness, sinus, ear ache.

•  Acetaminophen- 650mg
•  Ibuprofen- 200mg

•    Glucocorticoids- generally not needed 

•  Dexamethasone-  4mg
•  Methyl prednisolone- 4mg

•    Vit. C table

•    Zinc tablet (for loss of smell)

•    Antiviral therapy

•    Antibiotics therapy

PREVENTIONS

•    General hygiene should be maintained like washing hands.

•    Use alcohol containing sanitizer regularly

•    Avoid being close to infected person

•    Cover your mouth & nose while sneezing/coughing.

Red flags

• Difficult in swallowing & cough

Pearls

• Preventing aspects
• Social distance
• Maintain hand hygiene
• Arousal spread using mask

REFERENCE

•    Cooley, B. & McNeely, M. (1996). ETR Associates. Santa Cruz, CA.www.etr.org.

•   www.nature.com/news/commoncold 

•    World Health Organization(WHO)- viral diseases in India