SHOCK

BY:- DR K TARUN RAO

PG IN DEPT OF ORTHOPEDICS,

CAIMS

DEFINITION

• Shock is a state of poor perfusion with impaired cellular metabolism manifesting with severe pathophysiological abnormalities.

• It is due to circulatory collapse and tissue hypoxia.

• Normal aerobic metabolism is not maintained due to hypoperfusion.

STARLINGS FORCES

Causes of shock1. Hypovolaemic shock:- due to reduction in

total blood volume.

It may be due to:

a. Haemorrhage:-

– External from wounds, open fractures

– Internal from injury to spleen, liver, mesentery or pelvis

b. Severe burns, which results in loss of plasma

c. Peritonitis, intestinal obstruction

d. Vomiting and diarrhoea of any cause

2. Cardiac causes:-a. Acute myocardial infarction, acute carditis,b. Acute pulmonary embolismc. Drug inducedd. Toxaemia of any causese. Cardiac surgical conditions like valvular diseases,congenital heart diseases

f. Cardiac compression causes:-i. Cardiac tamponade due to collection of

blood, pus, fluid in the pericardial space which prevents the heart to expand leading to shock.

ii. Trauma to heart

3. Septic shock:— is due to bacterial infections which release toxins leading to shock

4. Neurogenic shock:— due to sudden anxious or painful stimuli causing severe splanchnic vessel vasodilatation. Here, patient either goes for cardiac arrest and dies or recovers fully spontaneously—spinal cord injury/anaesthesia can cause neurogenicshock

5. Anaphylactic shock:—is due to Type 1 hypersensitivity reaction

6. Respiratory causes:-

a. Atelectasis (collapse) of lung

b. Thoracic injuries

c. Tension pneumothorax

d. Anaesthetic complications

7. Other causes:-

a. Acute adrenal insufficiency (Addison‘s disease)

b. Myxoedema

Pathophysiology of ShockAny cause of shock

↓

Low cardiac output

↓

Vasoconstriction occurs as a compensation to perfuse vital organs like brain, heart, muscle, kidneys, liver

↓

Because of vasoconstriction and tachycardia

↓

Dynamic circulation increases

↓

Tachypnoea occurs to increase the oxygen saturation

↓

Peripheral veins (capacitance vessels constrictdiverting blood from splanchnic system towards essential vital organs

Decreased renal blood flow reduces the GFR and thereby the urine output

↓Renin angiotensin mechanism gets activated

causing further vasoconstriction and aldosterone release

↓Causes salt and water retention

↓ADH is released

↓Further concentration of urine occurs

When shock persists cardiac output falls further

Hypotension and tachycardia occurs leading to poor perfusion of coronaries

Hypoxia—metabolic acidosis

Release of cardiac depressants

Cardiac (pump) failure

Hypoxia

Anaerobic metabolism

Lactic acidosis

Cell wall damage

Sodium and calcium enterthe cell

Potassium leaks out of the cell

Causes hyperkalaemia, hyponatremia and hypocalcaemia

Intracellular lysosomes break down releasing powerful enzymes which destroy own cell

SICK CELL SYNDROME

Platelets are activated forming small clots in many places

Disseminated intravascular coagulation(DIC)(ConsumptionCoagulopathy)

Further bleeding.

Cerebral blood flow = cerebral perfusion pressure / cerebral vascular resistance

CPP is the difference between mean arterial pressure and intra cranial pressure.

EFFECTS OF SHOCK

Heart: Low perfusion → low venous return →

decreased cardiac output → hypotension → tachycardia. Persistent shock causes hypoxia and release of myocardial depressants leading to further cardiac damage.

• Lung: Interstitial oedema → decreased

gaseous exchange →pulmonary arteriovenousshunting → tachypnoea → Adult/Acute respiratory distress syndrome (ARDS) and pulmonary oedema.

Metabolic: Shock leads to hypoxia, which

activates anaerobic metabolism leading to lactic acidosis.

• Antidiuretic hormone (ADH) is released which increases the reabsorption of water from renal tubules. Other hormones released are ACTH, prostaglandins, histamine, bradykinin, and serotonin to compensate the effects of shock to increase the perfusion of vital organs like heart, brain and lungs.

Cellular changes:- occur in persistent shock due to release of lysosomal enzymes, which alters the cell membrane permeability causing cell death—sick cell syndrome.

Sympathetic:-overactivity alters the microcirculation leading to capillary dysfunction.

Brain:- perfusion, when decreases the patient becomes drowsy. Brain is the last organ to get underperfused in shock.

Kidneys: GFR decreases and tubular reabsorption of salt and water increases for compensatory response. But in severe cases tubular necrosis sets in leading into irreversible damage.

• Blood: Alteration in cellular components including platelets leads to Disseminated intravascular coagulation (DIC). It causes bleeding from all organs.

• Gastrointestinal tract: Mucosal ischaemiadevelops causing bleeding from GIT with haematemesis and malaena. It is aggravated by DIC. Hepatic ischaemia leads into increased enzyme levels.

Types of Shock

1. Vasovagal Shock and neurogenicshock:-

It is sudden dilatation of peripheral and splanchnic vessels causing reduced cardiac output and shock. Often it may be life-threatening due to hypoxia.

• Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger

Prior to losing consciousness, the individual frequently experiences early signs or symptoms such as lightheadedness, nausea, the feeling of being extremely hot or cold (accompanied by sweating),

• ringing in the ears (tinnitus), an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak or form words (sometimes combined with mild stuttering),

• weakness and visual disturbances such as lights seeming too bright, fuzzy or tunnel vision, black cloud-like spots in vision, and a feeling of nervousness can occur as well.

• The symptoms last for a few seconds before the loss of consciousness (if it is lost), which typically happens when the person is sitting up or standing.

• When sufferers pass out, they fall down (unless prevented from doing so) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness.

• . If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the blood's inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense. Fainting occurs with a loss of oxygen to the brain.

CAUSE

Typical triggers for vasovagal episodes include:

• Prolonged standing or upright sitting

• After or during urination (micturition syncope)

• Straining, such as to have a bowel movement or during vomiting

• Standing up very quickly (orthostatic hypotension)

• During or post-biopsy procedures

• Stress directly related to trauma[8]

• Stress

• Postural orthostatic tachycardia syndrome (POTS). Multiple chronic episodes are experienced daily by many patients diagnosed with this syndrome. Episodes are most commonly manifested upon standing up.

• Any painful or unpleasant stimuli, such as:

– Trauma (such as hitting one's funny bone)

– Watching or experiencing medical procedures (such as venipuncture or injection)

– High pressure on or around the chest area after heavy exercise

• Severe menstrual cramps

• Sensitivity to pain

• Arousal or stimulants (e.g. sex, tickling, or adrenaline)

• Sudden onset of extreme emotions

• Lack of sleep

• Hunger

• Coughing

• Being exposed to high temperatures

• Random onsets due to nerve malfunctions

TREATMENT1)Avoidance of trigger

2) Exposure-based exercises with therapists if the trigger is mental or emotional, e.g. sight of blood. However, if the trigger is a specific drug, then avoidance is the only treatment.

3) drinks with electrolytes

4) if they experience prodromal warning signs: they should lie down and raise their legs, or at least lower their head to increase blood flow to the brain. If the individual has lost consciousness, he or she should be laid down with his or her head turned to the side. Tight clothing should be loosened.

5) Wearing graded compression stockings may be helpful.

2. Neurogenic Shock:-

It is usually due to spinal cord injury, which cause dilatation of splanchnic vessels.

This type can safely be treated with vasoconstrictor drugs to bring up the blood pressure. There will be bradycardia, hypotension, arrhythmias, and decreased cardiac output.

• Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and can last up to 6 weeks

• Can be in response to spinal anesthesia

• Results in massive vasodilation leading to pooling of blood in vessels

• Blood pressure control, oxygen delivery, maintenance of haemodynamics, airway, fluid therapy, intravenous methylprednisolonetherapy should be done. Dopamine and /or phenylephrine (α agonist) can be used.

3. Hypovolaemic Shock— Most Common Type

Haemorrhage, may be due to injury to the liver, spleen,bone fractures, haemothorax, vascular injury, severe bleeding on table during surgeries of thyroid, liver, portalvein or major vessels. Vomiting, diarrhoea due to any cause, Burns.

4. Cardiogenic Shock:-

Cardiogenic shock is defined as circulatory failure causing diminished forward flow leading into tissue hypoxia in the setting of adequate intravascular volume with systolic blood pressure < 90 mmHg for 30 minutes; cardiac index < 2.2 L/minute / sq meter; raised PCWP (pulmonary capillary wedge pressure) > 15 mmHg. It is commonly seen in acute MI with. a mortality > 50

Cardiogenic shock develops within 24 hours of MI. it occurs when 50% of left ventricular wall is damaged by infarction. It leads to pulmonary oedema and severe hypoxia. Ischemic necrosis of left ventricular wall causes failure of pump thereby decreasing stroke volume

Diagnosis:- is established by ECG, echocardiography, arterial blood gas analysis, cardiac enzymes, PCWP and electrolyte estimation (hypokalaemia and hypomagnesaemia are common) are the essential investigations.

• Management:- Proper oxygenation with intubation, ventilator support, cardioversion, pacing, antiarrhythmic drugs, correction of electrolytes, avoiding fluid overload, prevention of pulmonary oedema as immediate measures.

• Dobutamine (β1 receptor agonist) is used to raise cardiac output provided there is adequate preload and intravascular volume (it is peripheral vasodilator and reduces BP).

Dopamine is preferred in patients with hypotension. But It may increase peripheral resistance and heart rate worsening cardiac ischaemia. Often both dopamine and dobutaminecombination may be required.

• Careful judicial use of epinephrine, norepinephrine, phosphodiesteraseinhibitors (amrinone, milrinone) are often needed. Anticoagulants and aspirin are given. Thrombolytics can be used. b blockers, nitrates (nitroglycerine causes coronary arterial dilatation), ACE inhibitors are also used.

Intra-aortic balloon pump (IABP) may

need to be introduced transfemorally as a mechanical circulatory support to raise cardiac output and coronary blood flow.

• Percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass graft (CABG) are the final choices.

Relief of pain, preserving of remaining myocardium and its function, maintaining adequate preload, oxygenation, minimizing sympathetic stimulation, correction of electrolytes should be the priorities.

5. Cardiac Compression Shock

• It is probably due to pericardial tamponade of any cause or kinking of great vessels, massive pulmonary embolism, tension pneumothorax, air embolism causes obstructive shock with reduced preload to heart.

Acute massive pulmonary embolism from a thrombus or an air embolism (50 ml of air), obstructing more than 50% of pulmonary vasculature leads to severe shock and sudden death.

Tachycardia, hypotension, pulmonary oedema, raised JVP, gallop rhythm are the features.

6. Septic Shock

Septic shock may be due to gram-positive organisms, gramnegative organisms, fungi, viruses or protozoalorigin.

Gram-negative septicaemia/gram-negative septic shock is called as endotoxic shock.

Gram positive septic shock• Due to exotoxin by gram

+ve bacteraemia like

Clostridium tetani/welchii,

staphylococci, streptococci

pneumococci

• Fluid loss, hypotension

is common; with normal

cardiac output

Gram negative septic shock• Gram negative bacteria

cause

• endotoxaemia and its effects.

• Urinary/gastrointestinal/

• biliary and respiratory foci are

• common

Pathophysiology of septic shock

Toxins/endotoxins from organisms like E. Coli, Klebsiella, Pseudomonas, and Proteus

Inflammation, cellular activation of macrophages, neutrophils, monocytes

Release of cytokines, free radicals

Chemotaxis of cells, endothelial injury, altered coagulation cascade—SIRS

Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea

Severe circulatory failure with MODS (failure of lungs,

kidneys, liver, heart) with DIC

Hypodynamic, irreversible cold stage of septic shock.

Septic shock is typically a vasodilatory shock wherein there is peripheral vasodilatation causing hypotension which is resistant to vasopressors. This is due to toxin induced release of isoform of nitric oxide synthetase from the vessel wall which causes sustained prolonged release of high levels of nitric oxide

Magnitude of infection is quantified as

(1) Sepsis which shows fever, tachycardia, leukocytosis

(2) Severe sepsis which shows low tissue perfusion with organ dysfunction (lactic acidosis, dysfunction of liver, kidney, lungs).

.

• (3) Septic shock with systemic hypotension (BP < 90 mm Hg in spite adequate fluid therapy), severe organ dysfunction (acute lung, kidney, liver injury), maldistribution of blood flow, shunting in microcirculation

Stages of septic shock

a. Hyperdynamic (warm) shock: This stage is

reversible stage. Patient is still having inflammatory response and so presents with fever, tachycardia, and tachypnoea

• . Pyrogenic response is still intact. Patient should be treated properly at this stage. Based on blood culture, urine culture (depending on the focus of infection), higher antibiotics like third generation cephalosporins, aminoglycosides, metronidazole are started.

• The underlying cause is treated like draining the pus, laparotomy for peritonitis, etc. Ventilatory support with ICU monitoring may prevent the patient going for the next cold stage of sepsis.

b. Hypodynamic hypovolaemic septic shock (cold septic shock): Here pyrogenic response is lost. Patient is in decompensated shock. It is an irreversible stage along with MODS (Multi-organ dysfunction syndrome) with anuria, respiratory failure (cyanosis), jaundice (liver failure), cardiac depression, pulmonary oedema, hypoxia, drowsiness, eventually coma and death occurs (Irreversible stage).

Treatment of septic shock

Correction of fluid and electrolyte by crystalloids, blood transfusion. Perfusion is very/most important.

Appropriate antibiotics—third generation cephalosporins/ aminoglycosides.

Treat the cause or focus—drainage of an abscess; wound excision

Pus/urine/discharge/bile/blood culture and sensitivity for antibiotics.

Critical care, oxygen, ventilator support, dobutamine/ dopamine/noradrenaline to maintain blood pressure and urine output.

Monitoring the patient by pulse oximetry, cardiac status, urine output, arterial blood gas analysis.

Short-term (one or two doses) high dose steroid therapy to control and protect cells from effects of endotoxaemia. It improves cardiac, renal and lung functions.

Single dose of methylprednisolone or dexamethasone which often may be repeated again after 4 hours is said to be effective in endotoxic shock.

Activated C protein(Drotrecogin alfa (Xigris))

prevents the release of inflammatory mediators and blocks the effects of these mediators on cellular function.

7. Anaphylactic ShockInjections—penicillins, anaesthetics,stings,

venom, shellfish may be having antigens which will combine with IgE of mast cells and basophils, releasing histamine and large amount of SRS-A (Slow releasing substance of anaphylaxis).

They cause bronchospasm, laryngeal oedema, respiratory distress, hypotension and shock. Mortality is 10%. Rashes all over the body are commonly observed.

TREATMENT

• Sudden onset

• ™. Distributive shock

• ™. Bronchospasm, laryngeal oedema

• ™. Generalised rashes and oedema

• ™. Hypotension, feeble pulse

• ™. Mortality 10%

• ™. To start adrenaline 100 ug IV, steroids, IV fluids, oxygen

• foot end elevation

• ™. Ventilator in severe cases

• ™. Cardiac massage, defibrillation

SHOCK(contd)

• DR A PAVAN KUMAR(PROF )

• DR CH RAMU (ASSOCIATE PROF)

• DR VAMSIDHAR REDDY(ASSISTANT PROF)

• DR G VENU(ASSISTANT PROF)

• DR SHASHI (ASSISTANT PROF)

• DR WASIM (ASSISTANT PROF)

HAEMORRHAGEClassification:-I. Based on the source of bleeding:

a. Arterial is bright red in colour, spurting like jet alongwith pulse of the patient.

b. Venous is dark red, steady and continuous flow. Bloodloss may be severe and rapid when bleeding is fromfemoral vein, jugular vein, other major veins, varicoseveins, portal vein, oesophageal varices.

Pulmonary arterial blood is dark red in colourand

pulmonary venous blood is bright red in colour.

c. Capillary: Here bleeding is rapid and bright red. It is often torrential due to continuous ooze.

II. Based on the time of onset of bleeding in relation to any operative procedure:

1. Primary: Occurs at the time of injury or operation.

2. Reactionary: It occurs within 24 hours after surgery or after injury (commonly in 4-6 hours). Anesthetic medics , and slipping of ligature.

3. Secondary: It usually occurs in 14 days after surgery. (heavily contaminated wound is closed primarily)

III. Based on the type of haemorrhage:

1) Revealed haemorrhage:- It is visible external haemorrhage

2) Concealed haemorrhage:- It constituted internal haemorrhage like liver injury, spleen injury, # femur, cerebral haemorrhage, hemothorax etc.

3) Initially concealed but later revealed haemorrhage:- hematuria, hemetemesis, melaena.

IV. Based on the duration of haemorrhage:

1. Acute haemorrhage: It is sudden, severe haemorrhage after trauma, surgery.

2. Chronic haemorrhage: It is chronic repeated bleeding for a long period like in haemorrhoids, bleeding peptic ulcer, carcinoma caecum, etc they present with chronic anaemia with hyperdynamic cardiac failure. (hemophilia)

They are in a state of chronic hypoxia. It is corrected by packed cell transfusion not by whole blood itself. Cause has to be treated accordingly.

3. Acute on chronic haemorrage: It is more dangerous as the bleeding occurs in individuals who are already hypoxic, which may get worsened faster.

Clinical Features of Haemorrhage

1)Pallor, thirsty, cyanosis.

2)Tachycardia, tachypnoea.

3)Air hunger.

4)Cold clammy skin due to vasoconstriction.

5)Dry face, dry mouth and goose skin appearance

(due to contraction of arrector pilorum).

6)Rapid thready pulse, hypotension.

7)Oliguria.

8)Features related to specific causes.

9)Shock index (ratio of pulse rate to blood pressure)

> 1 (cardiac index)

Measurement of Blood Loss

1) Clot size of a clenched fist is 500 ml.

2) Blood loss in a closed tibial fracture is 500-1500 ml; in a fracture femur is 500-2000 ml.

3)Weighing the swab before and after use is an important method of on-table assessment of blood loss.

4)Roughly 1kg soaked swab= 1000ml

Rains FactorTotal amount = of blood loss

Total difference in swab weight × 1.5or

Total difference in swab weight × 2(For larger wounds and larger operations)

Treatment1)Restoration of blood loss: By blood transfusion, albumin

4.5%, SAG-M blood, saline, Haemaccel (Gelatin), dextran,

plasma infusions.

Note: One unit of blood should raise 1 gm% of haemoglobin.

2) Catheterisation, foot end elevation, monitoring.

3)Oxygen support/intubation/ventilator and critical care.

4) Pressure, packing and head down (Trendelenburg) position to restore BP and blood supply of brain.

5)Wound exploration and proceeding, i.e. ligation of the small vessel, suturing the wound part, vessel suturing (anastomosis), excision of the tissues.

Trendelenberg position(Head down position)

6)Absolute rest, analgesics, morphine 10-20 mg IM/IV to relieve pain, sedation.

7)ICT placing for haemothorax.

8) Laparotomy for liver or spleen or mesentery or bowel injuries, suturing, splenectomy.

Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss)

9) Topical applications for local ooze—Oxycel, gauze soaked with adrenaline, bone wax for oozing from bone and other local haemostatic agents (collagen, thrombin).

10) In venous haemorrhage, elevation, ligation of vein or in case of large vein suturing of venous wall, pressure bandaging, packing will be helpful.

11)Tourniquet are often used in operation theatre for control of haemorrhage in limbs. But it is not advisable as a first aid measure.

12)TPN, CVP monitoring, electrolyte management are all equally important.

13) Steroid injection, antibiotics, ventilator support are often required.

Local haemostatic agents™

. Gelatin sponge (Gel foam)

™. Oxidised cellulose (Surgicel)

™. Collagen sponge (Helistat)

™. Microfibrillar collagen powder (Avitene)

™

. Topical thrombin

™. Bone wax (derived from bees wax + almond oil)

™. Gelatin matrices (Floseal)

™. Topical EACA, topical cryoprecipitate

ARTIFICIAL BLOOD

1. Perfluorocarbon (Fluosoleda)—abioticsubstitute as synthetic oxygen carrier. Its half life is 7 days. It is RBC substitute.

a)It has got high affinity for O2.

b)It is inert, colourless, odourless, dense, poorly soluble liquid.

c)It is biocompatible.

d)It is emulsified with albumin or lipids before infusion.

e)Its emulsion alone injection can cause pulmonary embolism.

f)It can bind and release oxygen. But as it reduces the PPO2 quickly, it is a disadvantage. Patient ideally to be kept in hyperbaric place.

2. Stroma free haemoglobin—biomimetichaemoglobin based substitute.

3. Chelates which reverse bound O2.

Intraoperative— salvage of blood: On table blood is collected, washed, filtered and transfused. Used in trauma.