Shock and homoeopathic management

Dr Daya Chandana

INTRODUCTION
It is very difficult to define shock in one sentence. Probably the best definition would be that ‘shock is a condition in which circulation fails to meet the nutritional needs of the cells and at the same time fails to remove the metabolic waste products’. It is a peripheral circulatory failure which results from a discrepancy in the size of the vascular bed and the volume of the intravascular fluid. It is a clinical condition which is characterized by signs and symptoms arising when the cardiac output is insufficient to fill the arterial tree with blood under sufficient pressure to provide all the organs and tissues with adequate blood flow. The low blood flow state in vital organs is the main cause of shock.

EPIDEMIOLOGY

The incidence of septic shock is 2-4% of admissions in western PICUs and 40-67% of admission in Indian PICUs.

Septic shock, a form of distributive shock, is the most common form of shock among patients admitted to the intensive care unit, followed by cardiogenic and hypovolemic shock; obstructive shock is rare. As an example, in a trial of 1600 patients with undifferentiated shock, septic shock occurred in 62 percent, cardiogenic shock in 16 percent, hypovolemic shock in 16 percent, other types of distributive shock in 4 percent (eg, neurogenic shock, anaphylaxis), and obstructive shock in 2 percent.

In the emergency department (ED), the percentage of each type of shock seen depends upon the population served by the ED. As an example, busy, urban, level-I trauma centers will see a higher percentage of hemorrhagic shock. In one study of 103 patients with undifferentiated shock presenting to a busy, urban ED, 36 percent of patients had hypovolemic shock, 33 percent had septic shock, 29 percent had cardiogenic shock, and 2 percent had other forms of shock.

ETIOLOGY

Shock is characterized by decreased oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization leading to cellular and tissue hypoxia. It is a life-threatening condition of circulatory failure and most commonly manifested as hypotension (systolic blood pressure less than 90 mm Hg or MAP less than 65 mmHg). Shock is the final manifestation of a complex list of etiologies and could be fatal without timely management. There are mainly four broad categories of shock: distributive, hypovolemic, cardiogenic, and obstructive. The wide range of etiologies can contribute to each of these categories and are manifested by the final outcome of shock. Undifferentiated shock means that the diagnosis of shock has been made; however, the underlying etiology has not been uncovered.

CLASSIFICATION
There are various types of shock, of which haematogenic or hypovolaemic shock is the most common and important. The various types of shock are as follows:

• Haematogenic or hypovolaemic shock.
• Traumatic shock.
• Xeurogenic shock.
• Cardiogenic shock.
• Septic shock.
• Miscellaneous types.

HYPOVOLAEMIC SHOCK

PATHOPHYSIOLOGY

Such shock is usually due to sudden loss of blood volume or loss of fluid from the vascular space. It is the haemorrhagic shock which is the most common form in this group and is discussed in details below:

Haemorrhage mostly occurs from the systemic venules and small veins which usually contain about 50% of the total blood volume. Loss of blood will cause decreased filling of the right heart. This causes decrease of filling of the pulmonary vasculature, which in turn decreases filling of the left atrium and ventricle. So left ventricular stroke volume also decreases by Frank-Starling mechanism. This causes a drop in arterial blood pressure.

COMPENSATORY MECHANISMS

The compensatory mechanisms which occur after haemorrhage include

• Adrenergic discharge.
• Release of vasoactive hormones.
• Resorption of fluid from the interstitial tissue.
• Resorption of fluid from the intracellular to the extracellular space.
• Renal conservation of body water and electrolytes.

ADRENERGIC DISCHARGE: It causes constriction of the venules and small veins, increase of heart rate and also constricts the vascular sphincters in the kidneys, splanchnic viscera and in the skin. Adrenergic discharge starts within 60 seconds after blood loss. Constriction of venules and small veins displaces blood to the right atrium and ventricle. This causes increase of the diastolic pressure of the right ventricle and also its stroke volume. This causes an increase of blood in the pulmonary vasculature and so into the left atrium and ventricle. Both left atrial and left ventricular fillings increase and so increases the left ventricular stroke volume. Adrenergic discharge constricts sphincters in the splanchnic viscera, kidneys and the skin. This selective vasoconstriction improves filling of the right heart and increases cardiac output. This also diverts blood to the heart and brain. So adrenergic discharge takes away a portion of the blood flow from the splanchnic viscera, kidneys and skin and diverts it to the heart and brain.

HYPERVENTILATION: This occurs in response to metabolic acidaemia which develops shortly after haemorrhage. Spontaneous deep breathing sucks blood from extrathoracic sites to the heart and lungs. This also increases the filling of left ventricle and. also its stroke volume. It must be remembered that both adrenergic discharge and hyperventilation occur within one minute of blood loss.

RELEASE OF VASOACTIVE HORMONES: Low perfusion of the kidneys leads to release of a hormone known as Renin from the juxtaglomerular apparatus. Renin liberates angiotensin I from the liver, which is converted to angiotensin II by the lungs. Angiotensin II is a potent selective vasoconstrictor. It selectively constricts the vasculature of the splanchnic organs, kidneys and the skin. So its vasoconstrictive effect is almost similar to that of adrenergic discharge.

After haemorrhage another vasoactive hormone, Vasopressin is released due to stimulus from the baroreceptors such as those situated in the carotid bodies and aortic arch caused by hypotension. Vasopressin acts as a systemic vasoconstrictor thus diverting blood to the brain and heart and increases cardiac output.

Epinephrine is also vasoactive hormone which is released from the adrenal medulla as a consequence of discharge of the adrenergic nervous system.

Release of vasoactive hormones usually takes place after 1 to 2 minutes of haemorrhage.

COLLAPSE: Assumption of the recumbent posture due to collapse automatically displaces blood from the lower part of the body to the heart and increases cardiac output.

RESORPTION OF FLUID FROM THE INTERSTITIAL TISSUE: Due to adrenergic discharge the arterioles, precapillary sphincters, postcapillary sphincters, the venules and the small veins of the skin and splanchnic organs and skeletal muscles constrict. This leads to decrease of the capillary intravascular hydrostatic pressure. This leads to influx of water, sodium and chloride from the interstitial tissue space into the capillaries.

RESORPTION OF FLUID FROM THE INTRACELLULAR TO THE EXTRACELLULAR SPACE: Release of epinephrine from the adrenal medulla, cortisol from the adrenal cortex and glucagon from the pancreas and inhibition of release of insulin all lead to high extracellular glucose concentration. Products of anaerobic metabolism also accumulate in the extracellular space. Both these cause hyper osmolarity of the extracellular tissue which draws water out of the cells. Interstitial pressure increases, which forces water, sodium and chloride across the capillary endothelium into the vascular space.

RENAL CONSERVATION OF BODY WATER AND ELECTROLYTES: Adrenocorticotropic hormone is released by any stress including shock. This hormone and angiotensin II stimulate the synthesis and release of hormone aldosterone from the adrenal cortex. Aldosterone is concerned with resorption of sodium from the glomerular ultrafiltrate into the vascular space. Reabsorption of sodium and water by the kidneys helps to maintain the vascular volume.

CLINICAL FEATURES

The clinical features of hypovolaemic shock depend on the degree of loss of blood volume and on the duration of shock.

• MILD SHOCK: Loss of less than 20% of blood volume is included in this category. The most sensitive clinical findings of shock are those caused by adrenergic constriction of blood vessels in the skin. The result is collapse of the subcutaneous veins of the extremities, particularly the feet which become pale and cool. There may be sweat in the forehead, hand and feet due to adrenergic discharge. Urinary output, pulse rate and blood pressure at this stage remain normal. The patient feels thirsty and cold.
• MODERATE SHOCK: Loss of blood volume from 20 to 40% causes this type of shock. Along with the other findings mentioned above, there will be oliguria. This oliguria is due to adrenergic discharge along with the effects of circulating aldosterone and vasopressin. The pulse is also increased but usually less than 100 beats per minute. In the initial stage the blood pressure remains normal but may fall in the later stage in the more severe group. Shock may be present even with normal pulse rate and normal blood pressure.
• SEVERE SHOCK: Loss of blood volume of more than 40% usually causes severe shock. At this stage there is pallor (skin of the extremities becomes pale), low urinary output, rapid pulse and low blood pressure.

TREATMENT
Mainly the treatment of haemorrhagic shock, which is the most common form of hypovolaemic shock, is discussed below. Though treatment of other types of shock are also described. The whole treatment can be described adequately under several heads.

1. RESUSCITATION: This should begin immediately as the patient is admitted with hypovolaemic shock. This starts with establishment of a clear airway and maintaining adequate ventilation and oxygenation. Lowering of the head with support of the jaw to prevent airway obstruction and administration of oxygen are usually all that are needed. Lowering of the head will improve venous return preventing stasis of blood in the muscles of the leg and preventing oedema. This also increases cerebral circulation which is quite important at this stage. In those patients where there is airway obstruction, intratracheal intubation and mechanical ventilation are required.

Many patients in shock, particularly those who are suffering from traumatic or septic shock require intubation and positive-pressure ventilation. Positive-pressure ventilation improves the patient’s cardiovascular status. Abrupt increase in airway pressure expands the alveoli and displaces blood from the pulmonary vasculature into the left atrium and ventricle. So both left ventricular output and systemic arterial pressure increase. But it must be remembered that positive-pressure ventilation is only applied when it is necessary otherwise it may compress the superior and inferior venae cavae and impair right atrial filling causing decrease in the right atrial stroke volume.

2. IMMEDIATE CONTROL OF BLEEDING is highly important in case of haemorrhagic shock. This may be achieved by raising the footend of the bed and by compression bandage to tamponade external haemorrhage. Operation may be required to stop such bleeding as soon as some resuscitation has been achieved.
3. EXTRACELLULAR FLUID REPLACEMENT is probably the most important point in the treatment of hypovolaemic shock. When the patients are admitted to the emergency room, a large-gauze needle or catheter is inserted into an appropriate vein (preferably in the arm or in the leg) and fluid should be administered immediately. Fluid replacement should be started immediately followed by the control of bleeding. In sophisticated centres another catheter is inserted into the subclavian and internal jugular vein to measure the CVP (Central Venous Pressure). A non-sugar, non-protein crystalloid solution with a sodium concentration approximately that of plasma is preferable in the initial stage of fluid replacement. That solution can be Ringer’s lactate, Ringer’s acetate or normal saline supplemented with 1 or 2 ampules of sodium bicarbonate. Ringer’s lactate or Ringer’s acetate solution should not be used in patients with severe pre-existing liver disease. This solution is run at a rapid speed so that in 45 minutes between 1000 and 2000 ml solution is given intravenously. It is often observed that blood pressure will return to normal and become stable after infusion of 1 or 2 litres of such solution. But it must be remembered that if blood loss has been severe or haemorrhage is continuing the elevation of blood pressure is usually transient. A sample of blood must be sent during insertion of the intravenous catheter for grouping and cross matching. Lactate acidosis has been reported with great concern by a few surgeons with the use of too much Ringer’s lactate solution. Further experiments have suggested that this is more theoretical than practical. Rapid administration of 5% glucose solution is never recommended, as this may induce osmotic diuresis, which further depletes patient’s vascular volume.

Resuscitation should always be started with crystalloid solution even if blood is available. If resuscitation is started with acidotic cold bank blood with a potassium concentration, efficiency of myocardium is tremendously jeopardized.

3 litres of fluid given over 45 minutes should resuscitate any patient with arrested haemorrhage. The need for more fluid indicates continuation of bleeding and such haemorrhage should be controlled surgically.

It is better to withhold administration of blood until surgical control of bleeding is obtained or at least until just before induction of anaesthesia. Rapid replacement of fresh blood after control of haemorrhage will lead to the fewest complications of coagulation and the least risk of transfusion complications.

At times when bleeding has been severe, blood should be given before surgical control of haemorrhage.

It must be remembered that blood substitutes like plasma or dextran should only be used when whole blood is not available. If whole blood is available these substances should not be infused before transfusing blood, as this may cause difficulty in cross matching and may inhibit the clotting system and exacerbate bleeding.

A few points to be remembered in case of extracellular fluid replacement:

1. The I.V. fluid, particularly the crystalloid, which should be given first, is administered with rapidity, so that replacement is done as quickly as possible without burdening the heart.
2. To know how much fluid should be given, blood pressure, pulse rate, urine output, CVP and other laboratory tests should be performed.
3. If there is blood loss, it is best replaced by blood. Blood substitutes cannot take the place of blood.
4. If blood is available, blood substitutes are better avoided.
5. DRUGS: A few drugs are sometimes used in different types of shock. These drugs are as follows:

• SEDATIVES: These drugs are commonly used to alleviate pain in patients with shock. Some amount of sedation is almost always required in any type of shock. Morphin is quite good in this respect and should be given intravenously, as subcutaneous injection may not yield its result due to poor absorption due to peripheral vasoconstriction. However it should not be administered in children, in head injury patients and in patients with acute abdomen, whose diagnosis has not been confirmed. For children berbiturates are preferred, whereas in head injuries largactil is a better choice. It must be remembered that treatment of pain is not obligatory from the stand point of shock itself. But if the patient is in severe pain as in fracture, peritonitis etc. control of pain is mandatory. Injection pethidine can also be used intramuscularly, but it has got slight vasodilator effect.
• CHRONOTROPIC AGENTS: The patients in shock who have slow heart rates may benefit from administration of chronotropic agents, which primarily increase the heart rate. This drug should probably be used selectively to patients with bradycardias. Atropine is the most widely used in this group, followed by isoproterenol. The latter drug has several beneficial effects in addition to that of increasing heart rate. It is also a vasodilator of the systemic arterial and capillary sphincters. It must be remembered that the adverse effects of administering these drugs should be compared with their beneficial effects. Rapid heart rates require increased myocardial work, which in turn requires increased coronary blood flow.
• INOTROPIC AGENTS: These drugs improve the strength of cardiac muscle contraction. Patients in cardiogenic shock and in severe septic shock may require such drug. The most commonly used drugs in this group are dopamine and dobutamine. These drugs in low doses increase myocardial contractility and selectively increase renal blood flow by dilating the renal vasculature. These drugs have also vasoconstrictor effect, so they should be used carefully and in low doses.
• VASODILATORS: Some patients in severe septic, traumatic and in cardiogenic shock may require these drugs. The most commonly used drugs in this group are nitroprusside and nitroglycerin, as these are easily reversible and short acting. When the systemic vascular resistance is too much raised, these drugs may be used. So these drugs are usually used in patients with high systemic mean arterial pressures. It should be remembered that excessive dilatation of the venules and small veins may decrease filling of the heart so that the cardiac output falls. Similarly excessive peripheral vasodilatation may lead to low systemic arterial pressures and decreased filling of the coronary vasculature which may be evidenced by electrocardiography. However administration of vasodilators to patients in shock with high systemic vascular resistances and high filling pressures of the heart seems to be an ideal therapeutic manoeuvre.
• VASOCONSTRICTORS: These drugs are particularly beneficial in neurogenic shock. The main role of these drugs in this condition is that they increase blood pressure and increase perfusion pressure for coronary circulation. These drugs also increase myocardial contractility. The drugs commonly used are phenylephrine and metaraminol. However these drugs are seldom used in hypovolaemic or traumatic shock.
• BETA-BLOCKERS: Patients in cardiogenic shock with stiff myocardium and rapid heart rate will benefit from administration of a beta-blocker. The drug increases efficiency of ventricular contraction. The drug however should be used with caution as it induces a slower heart rate. Propranolol is the most widely used drug in this group.
• DIURETICS: These drugs are sometimes used in treating patients with cardiogenic shock. These drugs reduce the vascular volume and decrease filling pressure. Diuretics should never be used in the initial treatment of patients with haemorrhagic or traumatic shock. Though oliguria is one of the main clinical manifestations of hypovolaemic shock, yet diuretics will not correct the underlying cause of oliguria, but will aggravate the situation by inducing further hypovolaemia. Diuretics are also not used in septic shock.

TRAUMATIC SHOCK

PATHOPHYSIOLOGY
The peculiarity of this shock is that traumatized tissues activate the coagulation system and release microthrombi into the circulation. These may occlude or constrict parts of pulmonary microvasculature to increase pulmonary vascular resistance. This increases right ventricular diastolic and right atrial pressures. Humoral products of these microthrombi induce a generalized increase in capillary permeability. This leads to loss of plasma into the interstitial tissue throughout the body. This depletes the vascular volume to a great extent.

CLINICAL FEATURES

Traumatic shock are almost similar to those of hypovolaemic shock. The two differentiating features are:

• presence of peripheral and pulmonary oedema in this type of shock and,
• Infusion of large volumes of fluid which may be adequate for pure hypovolaemic shock, is usually inadequate for traumatic shock.

TREATMENT

1. RESUSCITATION: In this type of shock mechanical ventilatory support is more needed.
2. LOCAL TREATMENT OF TRAUMA AND CONTROL OF BLEEDING: This is almost similar to hypovolaemic shock. Surgical debridement of ischaemic and dead tissues and immobilization of fractures may be required.
3. FLUID REPLACEMENT: As mentioned earlier more fluids should be required to bring back the patient to normalcy than hypovolaemic shock. Role of anticoagulation therapy to prevent disseminated intravascular coagulation has a debateable role. Increased coagulation consumes clotting factors of the blood leading to more bleeding. Moreover obstruction of microvasculature with such microthrombi lead to more tissue ischaemia. Anticoagulation with doses of heparin large enough to fully anticoagulate the patient may reverse this abnormality. The problem of this therapy is to calculate the dose. One intravenous dose of 10,000 units of heparin seems to be effective for this purpose.

CARDIOGENIC SHOCK

PATHOPHYSIOLOGY

It is usually due to primary dysfunction of one ventricle or the other (rarely of both). Such dysfunction may be due to myocardial infarction, chrortic congestive heart failure, cardiac arrhythmias, pulmonary embolism or systemic arterial hypertension. In cardiogenic shock caused by dysfunction of the right ventricle, the right heart is unable to pump blood in adequate amounts to the lungs. Filling of the left heart decreases. So left ventricular output decreases. In cardiogenic shock caused by dysfunction of the left ventricle, the left ventricle is unable to maintain an adequate stroke volume. Left ventricular output and systemic arterial blood pressure decrease. There is engorgement of the pulmonary vasculature due to normal right ventricular output, but failure of the left heart.

CARDIAC COMPRESSIVE SHOCK arises when the heart is compressed enough from outside to decrease cardiac output. The important causes are tension pneumothorax, pericardial tamponade and diaphragmatic rupture with herniation of the bowel into the chest.

CLINICAL FEATURES
In the beginning the skin is pale and cool and the urine output is low. Gradually the pulse becomes rapid and the arterial blood pressure becomes low. In case of right ventricular dysfunction the neck veins become distended and the liver may also be enlarged. In left ventricular dysfunction the patient has broncheal rales and a third heart sound is heard. Gradually the heart becomes enlarged and when the right ventricle also fails distended neck veins will be visible.

TREATMENT
Airway must be clear with adequate oxygenation. In case of right sided failure caused by a massive pulmonary embolus should be treated with large doses of heparin intravenously. If pain is complained of in case of left sided failure proper sedative e.g. morphin should be prescribed. Fulminant pulmonary oedema should be treated with a diuretic. Further treatment of cardiogenic shock is complex and beyond the scope of this treatise.

SEPTIC SHOCK

PATHOPHYSIOLOGY

During the past few years there has been a progressive increase in the incidence of septic shock. The importance of this shock is that it possesses a high mortality rate of about 50% or more. Even though this shock is now better understood and there are more potent antimicrobial agents available in the market, yet its mortality rate is still alarming.

The most frequent causative organisms are gram-positive and gram-negative bacteria, though any agent capable of producing infection (including viruses, parasites and fungi) may cause septic shock. Because of effective antibiotic treatment available for most gram-positive infections, the majority of cases of septic shock are now caused by gram-negative bacteria.

The common organisms which are concerned with septic shock are:

• coli
• Klebsiella aerobacter
• Proteus
• Pseudomonas and
• Bacteroids in order of decreasing frequency.

Recently Klebsiella groups are more isolated in cases of septic shock. Bacteroids which are difficult to culture may account for a far greater number of infections than was previously reported.

GRAM-POSITIVE SEPSIS AND SHOCK: This type of shock is usually caused by dissemination of a potent exotoxin liberated from gram-positive bacteria without evidence of bacteraemia. This is noticed more often in Clostridium tetani or Clostridium perfringens infections and fulminating infections from staphylococcus, streptococcus or pneumococcus organisms. Such shock is basically caused by massive fluid losses. Arterial resistance falls, but the peculiar feature is that there is little or no reduction in cardiac output even with progressive hypotension. Urine output is usually normal.

GRAM-NEGATIVE SEPSIS AND SHOCK: The most frequent source of gram-negative infections is the genitourinary system, often the patients had associated operations or instrumentations of the urinary tract. The second most frequent site is the respiratory system and many patients have had tracheostomy done. Third in frequency is the G.I. system with diseases such as biliary tract infections, intra-abdominal abscesses and peritonitis. Gram-negative sepsis as a cause of shock is a difficult problem. The severity of the shock varies considerably. There may be mild hypotension following instrumentation of the genitourinary tract. In contrast the patient with multiple intra-abdominal abscesses or necrotizing pneumonia may suffer from fulminating septic shock with poor prognosis. Outlook is more favourable when the source of infection is accessible to surgical drainage e.g. septic abortions.

CLINICAL FEATURES

Septic shock is often recognized initially by the development of chills and elevated temperature above 100°F. Two types are usually clearly defined — early warm shock and late cold shock.

In early warm shock there is cutaneous vasodilatation. The toxins from the infected tissues increase the body temperature. To bring this temperature down, the vasculature of the skin dilates. The cutaneous vasodilatation decreases systemic vascular resistance. So the arterial blood pressure falls, but cardiac output increases because the left ventricle has minimal resistance to pump against. Adrenergic discharge further increases cardiac output. In this stage the skin remains warm, pink and well perfused. The cutaneous veins remain full. The pulse rate becomes high and the systemic arterial pressure low. Diagnosis is not difficult as this condition is associated with intermittent spikes of fever alternating with bouts of chills.

In late cold shock there is increased vascular permeability due to liberation of toxic products into the centre circulation. This results in hypovolaemia and right heart filling decreases. Similarly there is decrease of flow into the pulmonary vasculature, so left heart filling decreases, so is the cardiac output. Clinically it may be difficult to differentiate this type of shock from hypovolaemic shock or from traumatic shock, only guide remains is the knowledge of existence of a septic focus.

TREATMENT

The only effective way to reduce mortality in septic shock is by prompt diagnosis and treatment. Treatment can be broadly divided into two groups:

• Treatment of infection by early surgical debridement or drainage and by use of appropriate antibiotics and
• Treatment of shock which includes fluid replacement, steroid administration and use of vasoactive drugs.
• Once a case of septic shock is diagnosed, thorough search for the source of infection is made while treatment of shock is started with fluid replacement. In sophisticated centres careful monitoring is started immediately with measure of central venous pressure, pulmonary wedge pressures by Swan-Ganz catheter, urine output and arterial and venous blood gases.

Debridement operation or drainage of infection should be performed under local or general anaesthesia as soon as possible after initial stability of the patient’s condition. This becomes easy when the infection is easily accessible. But problem remains when infective site is not so easily accessible. A patient with ascending cholangitis may respond temporarily to supportive treatment or shock therapy. This improvement is usually short-lived, unless prompt drainage of the biliary tract is performed.

The use of specific antibiotics based on appropriate culture and sensitivity test is desirable. Antibiotics must be chosen on the basis of the suspected organisms prior to the sensitivity results. Often a combination of antibiotics may be started in the beginning before getting the sensitivity result. When the report becomes available more specific antibiotic coverage should be instituted if the infection is not under control. Cephalothin (6 to 8 Gm/day I.V. in 4 to 6 divided doses), gentamicin (5 mg/Kg/day), clindamycin (particularly when infecting organism is Bacteroides) or chloromycetin (particularly in case of Bacteroides infection) are the antibiotics which may be started in the beginning.

• FLUID REPLACEMENT is of great importance in late septic shock. This will provide sufficient blood volume to the vital organs.

Mechanical ventilation along with endotracheal intubation is frequently needed in treating patients with late septic shock. Inadequate tissue oxygenation is a consistent feature of shock and attention to all components of the oxygen transport system is essential.

Steroids have been used for quite sometime in the treatment of septic shock, though its effectivity is still questioned. The serious question which has been asked that whether administering an agent that impaires the immune response of the body will be beneficial or not. On the other hand favourable responses with improvement in cardiac, pulmonary and renal functions and better survival rates have been reported with this therapy. It has been suggested that steroids protect the body cell and its contents from the effect of endotoxin.

Larger doses of steroids are known to exert inotropic effect on the heart and produce mild peripheral vasodilatation. Short term, high dose steroid therapy is recommended in most cases that do not respond to the other methods of treatment. An initial dose of 15 to 30 mg per Kg body weight of methyl prednisolone or equivalent dose of dexamethasone is given intravenously in 5 to 10 minutes. The same dose may be repeated within 4 hours if the beneficial effects have not been achieved. There is hardly a need for more than 2 doses. It has been shown that this short term high dose steroid therapy has little effect on immunosuppression, but possesses the other possible benefits to outweigh this bad effect.

VASOACTIVE DRUGS: The vasopressure drugs with prominent alpha-adrenergic effect are of limited value in treatment of this type of shock. Use of vasoactive drug with mixed alpha- and beta- adrenergic effects (e.g. metaraminol) may be indicated. Vasodilator drugs such as phenoxybenzamine are more popular particularly when combined with fluid administration. Inotropic agents e.g. isoproterenol or dopamine is ideal when simple volume replacement and other measures have failed to restore adequate circulation. Isoproterenol has inotropic and chronotropic effects on the heart and produces mild peripheral vasodilatation. This may cause a slight fall in blood pressure due to vasodilatation which requires additional volume replacement.

MIASMATIC APPROACH

SYCOSIS

• Rapid pulse
• Rapid breathing
• Cold clammy skin
• Nausea or vomiting
• Enlarged pupils
• Weakness or fatigue
• Dizziness or fainting
• Changes in mental status or behavior, such as anxiousness or agitation

REPERTORIAL APPROACH

BBCR

• CHEST-Congestion to: ACO., am-c., Aur., BELL., carb v., Chin., cocl., dig., fer., iod., Merc., nit-ac., NUX V., PHO., pul., tho.. thus, scil., seng, sep. Spo., SUL.
• CHEST- HEART AND REGION OF- Congestion to: Aco., am-c., asaf., asar., carb-v., cham., cyc., Fer., Glo., lau., lyc., merc-c., nit-ac., nuz-m., nux-v., pho., PUL., sep., sil., Sul.
• CHEST- HEART AND REGION OF- faint like, sensation: Arg-n., ars., op.
• BLOOD- PALPITATION in general: ACO., agar., alo., Alu., amb., am-c., anac., ang., ant-c.. ant-t., ap., apoc., arg-n.. arn., Ars., Asaf., asar., Aur., bar-c., Bell., bis.. bor., bov., Bro., Bry., buf., cact., CALC-C., cam., can., canth., carb-a., Carb-v., Caus., cham., chel., CHIN., cic., clem., Cocl., Cof., colch., colo., con., CROC., cup., cyc., dig., dul., euphr., Fer., gel., Glo., grap., grat., hell., hep., hyo., Ign., IOD., ip., kali-bi., Kali-c., kali-ch., Kali-n., kre., Lach., lau., led., lil-t., lith., LYC., lycps., mag-c., mag-m., mang., men., Merc., merc-c., mez., mos., mur-ac., naj., nat-c., NAT-M., nil-ac., nux-m., Nux-v., old., op., par., Petr., PHO., Pho-ac., plat., plb., pip-n., pod., pso., PUL., ran-s., rho., rhus-t., Rut., saba., sabi., samb., sang., sars., sec-c., sele., seng., SEP., sil., SPI., spo., stap., Stict., stra., stro., SUL., sul-ac., Tab., Thu., Val., Ver-a., verb., ver-v., vio-o., Vio-t., zin.
• RESPIRATION- quickened, rapid: ACO., agar., alu., amb., am-c., anac., ant-t., arn., ars., asaf., asar., aur., bar-c., BELL., bor., bov., BRY., calc-c., cam., can., canth., carb-a., CARB-V., caus., cham., chin., cic., CINA, cocl., cof., colo., con., CUP., cyc., dig., dro., euphor., euphr., fer., guai., hell., HEP., hyo., ign., IOD., IP., kali-bi., kali-c., kali-n., kre., lach., Lau., led., LYC., mag-c., mag-m., merc., mez., nux-m., mos., nut-c., nat-m., nit-ac., NUX-V., op., petr., PHO., pho-ac., plat., plb., PUL., ran-b., rho., rhus-t., rut., saba., sabi., Samb., sars., scil., sec-c., seng., SEP., sil., spi., Spo., stan., stap., vio-o., zin., stra., SUL., VER-A.
• CIRCULATION- PULSE- quick (accelerated): ACO., Agar., Alu., AMB., AM-C., AM-M., ANAC., Ang., ant-c., ANT-T., AP., Arg., ARN., ARS., ASAF., ASAR., AUR., BAR-C., bar-m., BELL., bis., BOR., BOV., BRO., BRY., CALC-C., cam., can., CANTH., CARB-A., Carb-v., caus., CHAM., CHEL., CHIN., CINA., Clem., Cocl., Cof., COLCH., COLO., Con., CROC., Cup., dig., fer., Flu-ac., glo., grat., GUAI., HEP., HYO., IGN., IOD., IP., kali-bi., Kali-c., KALI-N., kre., LACH., Lau., LED., Lyc., Lycps., Mag-c., Mag-m., Mang., Mar., Men., MERC., merc-c., mez., MOS., naj., NAT-C., NAT-M., Nit-ac., Nux-m., NUX-V., Old., Op., par., PETR., PHO., PHO-AC., Plb., PUL., Ran-b., Ran-s., Rhe., RHUS-T., Rut., sabi., samb., Sars., Sec-c., Sele., SENG.

HOMOEOPATHIC MANAGEMENT

• ACONITE NAPELLUS: Palpitation of the heart, with great anxiety, heat of body, chiefly in the face, and great weariness in the limbs. Shootings in the region of the heart when moving or going upstairs. Sensation of compression and blows in the region of the heart. Inflammation of the heart. Chronic diseases of the heart, with continuous pressure in the left side of the chest, oppressed breathing when moving fast and ascending steps, stitches in the region of the heart, congestions to the head; attacks of fainting and tingling in the fingers. Fainting with tingling. Pulse full, strong, hard; slow, feeble; threadlike with anxiety; quick, hard, small.
• ACTEA SPICATA: Difficult inspiration; stitches in epigastrium during deep breathing or a painful shock; or pain in the hip. Urging sensation in heart towards abdomen and region of liver, with great anxiety at night. Pulse 120.
• ARNICA MONTANA: Coughs depending on cardiac lesion, paroxysmal, at night, during sleep, worse exercise. Acute tonsillitis, swelling of soft palate and uvula. Pneumonia; approaching paralysis. Hoarseness from overuse of voice. Raw, sore feeling in morning. Cough produced by weeping and lamenting. Dry, from tickling low down in trachea. Bloody expectoration. Dyspnoa with hæmoptysis. All bones and cartilages of chest painful. Violent spasmodic cough, with facial herpes. Whooping cough, child cries before coughing. Pleurodynia. Angina pectoris; pain especially severe in elbow of left arm. Stitches in heart. Pulse feeble and irregular. Cardiac dropsy with distressing dyspnoea. Extremities distended, feel bruised and sore. Fatty heart and hypertrophy.
• ARSENICUM ALBUM: Beating, and palpitation of the heart. Pain from liver up through left chest and down left arm, veins of hands swollen, purplish; sudden pain as if heart squeezed or had got a shock (angina pectoris). Heart strained; irritable; stitches in; from left to right Painful pricking in the heart, with fainting fits.
• CROTALUS HORRIDUS: Much pain in heart, through left shoulder-blade and down left arm. Palpitation with sore pain in and about heart; feeling as if heart tumbled over. Heart tender when lying on left side. Pulse hardly perceptible.
• DIGITALIS PURPUREA: Desire to take a deep breath. Breathing irregular, difficult; deep sighing. Cough, with raw, sore feeling in chest. Expectoration sweetish. Senile pneumonia. Great weakness in chest. Dyspnea, constant desire to breathe deeply, lungs feel compressed. Chronic bronchitis; passive congestion of the lungs, giving bloody sputum due to failing myocardium. Cannot bear to talk. Haemoptysis with weak heart. The least movement causes violent palpitation, and sensation as if it would cease beating, if he moves. Frequent stitches in heart. Irregular heart especially of mitral disease. Very slow pulse. Intermits; weak, Cyanosis. Inequality of pulse; it varies. Sudden sensation as if heart stood still. Pulse weak, and quickened by least movement. Pericarditis, copious serous exudation. Dilated heart, tired, irregular, with slow and feeble pulse. Hypertrophy with dilatation. Cardiac failure following fevers. Cardiac dropsy.
• STRONTIUM CARBONICUM: Chronic sequelae of haemorrhages, after operations with much oozing of blood and coldness and prostration. Arterio-sclerosis. High blood pressure with flushed face pulsating arteries, threatened apoplexy. Violent involuntary starts. Affections of bones, especially femur. Restlessness at night, smothering feeling. For shock after surgical operations. Neuritis, great sensitiveness to cold.
• TABACUM: Palpitation when lying on left side. Pulse intermits, feeble, imperceptible. Angina pectoris, pain in praecordial region. Pain radiates from center of sternum. Tachycardia. Bradycardia. Acute dilatation caused by shock or violent physical exertion. Legs and hands icy cold; limbs tremble.
• THEA CHINESIS: Oppressed; constricted; fluttering in left side with fulness about clavicles, and feeling, of suffocation; tight across upper part compelling her to sit up in bed. Anxiety in precordium. Anxious oppression, anguish. Spasm in region of heart. As if on the verge of fainting. Palpitation; violent. Pulse: full, quick; feeble, irregular, intermittent.
• VERATRUM ALBUM: A perfect picture of collapse, with extreme coldness, blueness, and weakness, is offered by this drug. Post-operative shock with cold sweat on forehead, pale face, rapid, feeble pulse. Cold perspiration on the forehead, with nearly all complaints. Vomiting, purging, and cramps in extremities. The profuse, violent retching and vomiting is most characteristic. Surgical shock. Excessive dryness of all mucous surfaces. “Coprophagia” violent mania alternates with silence and refusal to talk.

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