Shock Management

Each variety of shock has to be elucidated and managed slightly differently, as the etiology and pathology are different, in various types of shock

"Fluid therapy is goal directed therapy and in septic shock it should be adequately done in the first six hours" - Dr S Manimala Rao Chief Intensivist HOD-Anaesthesiology Yashoda Hospital Hyderabad

Understanding the patho physiology and the types of shock one encounters in clinical practice is the hallmark of management. Each variety of shock has to be elucidated and managed slightly differently as the etiology and pathology are different in various types of shock. However, the basic management is somewhat similar centering around resuscitation and treating the cause. Shock is defined as a clinical state with characteristic symptoms and signs that occurs due to an imbalance between oxygen supply and demand. This in turn leads to tissue hypoxia.

Pathophysiology

Shock is classified according to the etiology. It is hypovolemic, when the blood/fluid volume is depleted, due to innumerable causes. It is cardiogenic, if there is an underlying cardiac disease. It is septic or distributive when there is septic pathology. Anaphylactic due to drug or insect bite allergy. It is neurogenic, when the cause is neurological insult. In practice, however, there is considerable overlap between the different types of shock It may not be uncommon to find different varieties in the same patient at a given time. By understanding the oxygen uptake and delivery, one can understand the subject of shock more clearly.

The oxygen delivery is nothing but the O2 flux calculated from cardiac output and oxygen carriage represented by haemoglobin content and saturation (DO2). The normal O2 extraction ratio is 5ml/ dl. The tissues maintains the O2 uptake in hypovolemia by extracting more of O2 and maintains the level at 14ml/kg /minute which till this level is supply independent VO2. Once the DO2 falls below a critical value of 8-10 ml/kg/min, this compensatory mechanism is not sufficient and O2 uptake begins to fall. Then, the VO2 becomes supply dependent. This phase is associated with accumulation of oxygen debt. The blood lactate levels rise and they can estimate the severity of shock.

Septic Shock

In septic shock, due to bacterial, viral or fungal, the pro-inflammatory mediators as well as anti-inflammatory mediators are released and complement activation results. This could lead to increase in cytokines, arachadonic acid metabolites and release of oxygen free radicals and nitric oxide. There could be relative adrenal insufficiency as well as depletion of vasopressin stores- leading to vasodilatory shock in spite of high cardiac output. Despite of high cardiac output there is tissue hypoxia. There is reduced intravascular volume due to increased capillary permeability. DO2 may be supra normal and Vo2 may be normal. There is lactic acidosis, reduced perfusion leading to organ dysfunction.

Sepsis-induced mitochondria dysfunction may prevent the oxygen utilisation at cellular level. In all varieties of shock, the ultimate is failure of oxygenation at cellular level and if not corrected leads to failure of sodium and potassium pumps, anaerobic metabolism leading to lactic acidosis and worsening of the situation. Uncoupling of oxidative phosphorylation leads to decreased cardiac contractility. The addition of myocardial depressant factor can definitely decrease the contractility and thereby reduce perfusion to all organs leading to multi-organ failure. The increased coagulation and inflammation lead to micro thrombi formation and ultimately proceeds to multiple-organ dysfunction syndrome with high mortality.

Patients in hypovolemic and cardiogenic shock usually have low cardiac index. The blood pressure may be low or normal in the beginning due to compensatory vasoconstriction. Tachycardia, confusion, tachypnoea, oliguria may be present. Presence of rales crepitations, severe dyspnoea may indicate cardiogenic shock. History of cardiac disease, hepatojugular reflex, jugular venous pulse and high CVP will aid in the diagnosis of cardiogenic shock. Whereas cold periphery, peripheral cyanosis, pallor may denote hypovolemic shock. History of volume loss, trauma and GI losses with low CVP may show the way towards hypovolemia.

Septic shock, on other hand, has high cardiac index but low blood pressure, in spite of fluid resuscitation. There could be a proven sepsis. Requirement of vasopressors even after adequate fluid replacement. Vasopressin may be required in some patients. Usually, there is hypotension, tachycardia, warm periphery and bounding pulse as well as lactic acidosis along with one or more organ failure. History and physical examination still are in the forefront, as the patient is being resuscitated and arrive at tentative diagnosis

Lab data are very helpful. Besides, the routine investigations like Hb, Pcv, total white cell count and coagulation parameters, the blood lactate and procalcitonin levels, blood cultures can be utilised to diagnose septic shock. Troponin estimation, Bnp levels, ECG, X-ray chest, an echo cardiogram, arterial blood gasses are sufficient to confirm the diagnosis in cardiogenic shock. Echo can also give an idea to differentiate between the septic and cardiogenic entity. Pulmonary embolism can be diagnosed from history, ultrasound, Doppler and pulmonary CT angiography.

Haemodynamic Monitoring

Routinely central venous and arterial pressures are measured, Svco2 monitoring in septic shock as in goal directed therapy. Cardiac output monitoring is helpful in cardiogenic and septic shock. Any of the recent methods not utilising the pulmonary artery insertion are utilised as the need be.

Shock Management

General measures: Fluids, warmth, oxygenation with high flow oxygen. If patient is not restless, one can try non-invasive ventilation to reduce the work of breathing. Keep the fluid from the alveoli and improve oxygenation. Resuscitation and investigation can proceed simultaneously.

If the patient is restless and has altered sensorium with ABG showing a PAO2/FIO2 less than 300, one may have to intubate and ventilate these patients. If the ratio is less than 200, one can go directly to pressure controlled mode and recruit the lungs at the earliest. Intubation and sedating the patients also helps to insert the monitoring lines safely. Inserting them in delirious patients in shock, can be difficult and end up in higher complications. Fluid therapy is goal directed therapy and in septic shock it should be adequately done in the first six hours. Targeting a Hb level of 10gms and an SVCo2 of 70 per cent showed a16 per cent decrease in mortality.

Appropriate antibiotics, vasopressin and steroids are used to improve mean arterial pressures. When indicated, activated protein C has shown to reduce the mortality, but is an expensive drug and should be used with caution as it can cause haemorrhage and should be used in correctly selected patients within 24- 48 hours.

In uncomplicated hypovolemic shock, CVP monitoring is sufficient to guide the fluid therapy. It should correct the deficit and if there is loss of blood and factors, they should be corrected accordingly. Urgent control of bleeding is the most important aspect of management. Crystalloids first and less than 10-15ml/kg colloids are quite efficient in managing most situations. Hyper tonic solutions are used in specific situations. Blood is usually given as a red cell concentrate. This can be combined with either crystalloid colloid or albumin. The crystalloid and colloid controversy continues, but crystalloids continue to be the fluid of choice.

Inotropic Support

Inotropic support is rarely required in hypovolemic shock, if fluid resuscitation is adequate. However, it may be necessary to start as the fluid is being infused to keep up the pressure. In circumstances where there is an uncontrollable haemorrhage one may even consider permissive hypo tension. Fluid resuscitation and control of bleeding are the key points for better outcomes. Vasopressors and inotropic drugs are required in septic and cardiogenic shock. Judicious and titrable doses have to be employed. The latter may require an inodilator. A combination of dobutamine and nor adrenaline is suited in septic shock and vasopressin and steroids are added as and when indicated according to the evidence.

Low volume ventilation and strict glycemic control are the few evidences which are practiced for septic shock and other forms for better outcomes. Cardiogenic shock may require in IABP and PTCA /CABG.

Dopamine is still used as one of the first line of inoconstictor. The side effects are many. The adverse effects on pulmonary function, cell function, gut mucosal perfusion. Renal dose of dopamine is not given as the evidence shows no benefit. If and when natriuresis is required, it can be achieved by frusemide in 10-80 mg doses as bolus or infusion of 3-10mg per hour after adequate volume replacement.

Outcome of shock depends upon how quickly the patient is brought to the correct place for resuscitation and management. A protocolised approach starting at the earliest and practicing evidence-based medicine to manage these patients in emergency and intensive care departments is essential. The outcomes also depend on the associated co-morbid conditions, extremes of age, response to therapy. Hypovolemia has better outcomes than septic or cardiogenic shock.

Anaphylactic Shock

The other variety of shock is anaphylactic, which is mainly due to anaphylaxis. The most severe type of anaphylaxis, occurs when an allergic response triggers a quick release from mast cells of large quantities of immunological mediators histamines, prostaglandins, leukotrienes leading to systemic vasodilation associated with a sudden drop in blood pressure and edema of bronchial mucosa- resulting in bronchoconstriction and difficulty breathing. Anaphylactic shock can lead to death in a matter of minutes if left untreated.

Researchers typically distinguish between 'true anaphylaxis' and 'pseudo-anaphylaxis.' The symptoms, treatment, and risk of death are identical, but 'true' anaphylaxis is always caused directly by degranulation of mast cells or basophils that is mediated by Immunoglobulin E (IgE). Pseudo-anaphylaxis occurs due to all other causes. The distinction is primarily made by those studying mechanisms of allergic reactions. Adrenaline (epinephrine) is the drug most commonly used to treat anaphylactic reactions. If necessary, a doctor or emergency medical team may perform Cardio Pulmonary Resuscitation (CPR). They may also administer intravenous antihistamines and cortisone to reduce inflammation of air passages and improve breathing.

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