- In shock, inadequate blood flow results in inadequate oxygen delivery to tissues, affecting cell function and leading to a series of stages: initial, compensatory, progressive, and refractory.
- The compensatory stage involves physiological mechanisms like hyperventilation, vasoconstriction, and hormonal responses such as the release of adrenaline and noradrenaline to reverse the condition.
- In the progressive stage, compensatory mechanisms begin to fail, leading to metabolic acidosis, tissue damage, and fluid leakage due to prolonged vasoconstriction.
- The refractory stage occurs when vital organs fail, and death is imminent, with shock being a continuous complex condition with no sudden transition between stages.
- Types of shock include hypovolemic, cardiogenic, distributive (like septic shock and anaphylactic shock), neurogenic, obstructive, endocrine, hypovolemic, and psychogenic shock, each with specific causes and effects on the body.
- Septic shock is characterized by circulatory insufficiency due to bacterial products interacting with host cells, leading to a widespread unregulated host response and a high mortality rate.
- Sepsis and septic shock can present with systemic inflammatory responses, organ dysfunction, hypoperfusion, and various symptoms such as fever, chills, altered mental status, and localized infection-related symptoms.
- Symptoms of shock include changes in blood pressure and pulse rate, altered sensorium, skin changes, thirst, decreased urine output, and other signs that vary depending on the type of shock present.- Restlessness and altered mental state can be caused by decreased cerebral perfusion due to subsequent hypoxia
- Signs of shock can include a rapid, weak, thready pulse, cool clammy skin, and vasoconstriction
- Fluid depletion from shock can lead to thirst, dry mouth, and fatigue due to inadequate oxygenation
- Shock is not just low blood pressure, a falling blood pressure is a late sign of shock
- Factors affecting response to shock treatment include the magnitude of insult, patient's health, age, temperature extremes, altitude, humidity, fear, pain, hydration status, nutrition, pre-existing diseases, and drugs taken by the patient
- The goal of shock treatment is to restore normal tissue perfusion by monitoring blood pressure, pulse, respirations, skin appearance, sensorium, urine output, hemoglobin, and hematocrit
- Treatment of shock involves securing and maintaining the airway, applying high concentration oxygen, assisting with ventilations if needed, controlling bleeding, stabilizing fractures, preventing loss of body heat, and elevating lower extremities
- Inotropic support may be considered in shock treatment, and determining the type of fluid to use can vary depending on the situation
- Types of shock treatment vary based on the type of shock, such as hypovolaemic shock or cardiogenic shock
- Effective treatment for shock may involve early recognition, rapid resuscitation, and addressing both hemodynamic and inflammatory components
- Blood transfusions can have both good effects, like restoring blood volume and increasing oxygen delivery, and bad effects, such as transfusion reactions and disease transmission
- Different types of shock, such as hypovolaemic shock and cardiogenic shock, require specific treatments like fluid replacement and inotropic agents, respectively
- Specialized treatment approaches are needed for various types of shock, such as distributive, obstructive, neurogenic, and endocrine shock
- Control of external bleeding involves methods like direct pressure, elevation, arterial pressure point compression, splinting, or using tourniquets as a last resort
- Epistaxis, or nosebleeds, are a common problem that can be managed by sitting up, leaning forward, applying pressure, and applying ice
- Internal bleeding can result from trauma, clotting disorders, or organ rupture, and management involves controlling external bleeding, stabilizing fractures, and transport
- The prognosis of shock depends on the underlying cause and extent of concurrent issues, with septic shock having a higher mortality rate and cardiogenic shock having a worse prognosis
- Quick treatment is essential for a good prognosis in cases of shock, especially hypovolaemic shock which can cause serious complications if not promptly managed
- Recognizing occult hemorrhage, avoiding assumptions in trauma cases, and providing adequate resuscitation are important considerations in managing shock, especially in different age groups like pediatric and geriatric patients.- Responses to certain stimuli or situations can lead individuals to seek therapy for support and coping mechanisms.
Shock in Otolaryngology : Concepts and Applied Aspects
Definition of Shock
“a rude unhinging of the machinery of life.” (1852)
Recent definition-
“the collapse and progressive failure of the cardiovascular system.”
Inadequate perfusion (blood flow) leading to inadequate oxygen delivery to tissues.
Fatal.
Recognized and treated immediately.
Systemic hypoperfusion either due to decreased cardiac output or low circulating blood volume
PATHOPHYSIOLOGY
Effects of inadequate perfusion on cell function.
STAGES OF SHOCK
Initial Stage
Hypoxia
Compensatory stage
Acidosis
Progressive stage
Efflux of K+ and Influx of Na+
Refractory stage
Vital organs damage
Death will occur imminently.
Shock is a complex and continuous condition.
No sudden transition from one stage to the next.
Compensatory (Compensating)
This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline. Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin-angiotensin axis is activated and arginine vasopressin is released to conserve fluid via the kidneys. Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin-angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.
Progressive (Decompensating)
Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar and precapillary sphincters constrict such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.
Refractory
At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently. Shock is a complex and continuous condition and there is no sudden transition from one stage to the next.
Types of Shock and Their Causes
Hinshaw and Cox, 1972.
Hypovolaemic shock –
Cardiogenic shock –
Intrinsic
Myocardial injury
Tachycardia
Bradycardia
Valvular defect
Extrinsic
Pericardial tamponade
Tension pneumothorax
Large pulmonary emblous
Distributive shock
Insufficient intravascular volume of blood.
“Relative" hypovolaemia .
Examples:
Septic shock –
Gram negative bacteria i.e. Escherichia coli, Proteus species, Klebsiella pneumoniae : release an endotoxin .
Gram-positive cocci- pneumococci and streptococci.
Fungi as well as Gram-positive bacterial toxins produce a similar syndrome.
Anaphylactic shock
Allergen, antigen, drug or foreign protein
Release of histamine – vasodilation-hypotension and increased capillary permeability.
Neurogenic shock
rarest form of shock.
Trauma to the spinal cord
resulting in the sudden loss of autonomic and motor reflexes below the injury level.
Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance, leading to vasodilation and hypotension.
Obstructive shock
circulatory arrest.
Several conditions result in this form of shock.
Cardiac tamponade
Constrictive pericarditis
Tension pneumothorax.
Massive pulmonary embolism.
Aortic stenosis
Endocrine shock
Hypothyroidism, reduces cardiac output.
Thyrotoxycosis -reversible cardiomyopathy.
Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment without tapering the dosage.
Relative adrenal insufficiency.
Hypovolemic Shock
Medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate perfusion.
Causes
Blood loss: trauma
Plasma loss: burns
Water loss: Vomiting, diarrhea, sweating, increased urine, increased respiratory loss
Psychogenic Shock
Simple fainting (syncope)
Caused by stress, pain, fright
Heart rate slows, vessels dilate
Brain becomes hypoperfused
Loss of consciousness occurs
Anaphylactic Shock
Results from severe allergic reaction
Body responds to allergen by releasing histamine
Histamine causes vessels to dilate.
Neurogenic Shock
Failure of the nervous system to control diameter of blood vessels
Causes pooling of blood and there is generally no actual blood loss
Classic signs of shock may not be present
Septic Shock vs. SIRS
Systemic Inflammatory Response Syndrome (SIRS) physiologic alternations and organ dysfunction seen with bacterial infections
Results from body’s response to bacteria in bloodstream.
(Pittet et al,1995).
158 patients (93%) had SIRS for an incidence of 542 episodes/1000 patients-days.
The incidence of SIRS in the ICU was even higher (840 episodes/1000 patients-days).
83 patients (49%) had sepsis; among them 28 developed severe sepsis.
Importantly, 13 patients had severe sepsis after discharge from the ICU.
Septic Shock vs. SIRS
Sepsis
systemic host response to infection with SIRS plus a documented infection
Severe Sepsis
sepsis plus end-organ dysfunction or hypoperfusion
Septic Shock
sepsis with hypotension, despite fluid resuscitation with evidence of inadequate tissue perfusion
1992
Heart rate > 90 beats per minute
Body temperature < 36 or > 38°C
Tachypnea (high respiratory rate) > 20 breaths per minute or, on blood gas, a PaCO2 < 4.3 kPa (32 mm Hg)
White blood cell count < 4000 cells/mm³ or > 12000 cells/mm³ (< 4 x 109 or > 12 x 109 cells/L), or the presence of greater than 10% immature neutrophils.
Causes of SIRS
Severe trauma
Complications of Surgery,
Burns
Acute pancreatitis
Immunodeficiency (such as AIDS[6])
Complication of SIRS
SIRS can result
multiple organ dysfunction syndrome.
Hypotension related to vessel dilation
Hypovolemic Shock
Septic Shock: Pathophysiology
circulatory insufficiency occurs when bacterial products interact with host cells
serum proteins - initiate reactions.
cell injury and death.
widespread and unregulated host response to these substances also results in the elaboration or an extensive array of chemical mediators.
Septic Shock: Pathophysiology
Has 25-75% mortality,
1,00,000 deaths in ICU per annum in US.
Septic shock develops in less than one half of patients with bacteremia.
It occurs in 40% -gram-negative bacteremia
20% of those patients with Staphylococcus aureus bacteremia.
Septic Shock: History
􀂇 Fever
􀂇 Chills
􀂇 Sweating
􀂇 Altered mental status
􀂄 Apprehension
􀂄 Anxiety
􀂄 Agitation
Localizing symptoms
Head and neck infections - earache, sore throat, sinus pain or congestion, nasal congestion or exudate, swollen lymph glands
Chest and pulmonary infections - cough (especially if productive), pleuritic chest pain, dyspnea
Abdominal and GI infections - abdominal pain, nausea, vomiting, diarrhea
Pelvic and genitourinary infections - pelvic or flank pain,
vaginal or urethral discharge, dysuria, frequency, urgenc
Bone and soft tissue infections - focal pain or tenderness, focal erythema, edema
Signs and Symptoms of Shock
Hard-core measurements
ô€‚‡ Blood pressure changes ↑ or
↓
ô€‚‡ Pulse rate ↑ or ↓
ô€‚‡ Hemoglobin / hematocrit ↓
or NL
ô€‚‡ Urine output ↓
􀂇 Electrocardiogram
􀂇 Arterial blood gas
􀂇 **Pulmonary artery wedge
pressure
􀂇 **Cardiac output
􀂇 **Cardiac index
􀂇 ** Central venous pressure
Soft-core measurements
􀂇 Skin changes (cool, pale or
damp)
􀂇 Altered Sensorium (depressed or apprehensive)
􀂇 Thirst
􀂇 Vein changes
􀂇 Hyperventilation
􀂇 Obvious or occult blood loss
** requires invasive monitoring
Shock:
Signs and Symptoms
Restlessness, anxiety
Decreasing level of consciousness
Dull eyes
Rapid, shallow respirations
Nausea, vomiting
Thirst
Diminished urine output
Shock:
Signs and Symptoms
Hypovolemia will cause
Weak, rapid pulse
Pale, cool, clammy skin
Anxiety and restlessness
Hypotension
Cardiogenic shock may cause:
Weak, rapid pulse or weak, slow pulse
Pale, cool, clammy skin
Neurogenic shock will cause:
Weak, slow pulse
Dry, flushed skin
Sepsis and anaphylaxis will cause:
Weak, rapid pulse
Dry, flushed skin
Shock:Signs and Symptoms
Patients with anaphylaxis will:
Develop hives (urticaria)
Itch
Develop wheezing and difficulty breathing (bronchospasm)
Shock:
Signs and Symptoms
Factors Effecting Response to Shock and Treatment
Magnitude of insult
Health of patient
Age
Temperature
extremes (hot or cold)
Altitude
Humidity
Fear
Pain
Hydration status
Nutrition
Pre-existing diseases
Drugs taken by patient
Treatment of Shock:
Goal
Success depends on
early recognition of shock
rapid tempo of resuscitation of its hemodynamic component to prevent or minimize the inflammatory component. (Holmes et al,2003).
TO RESTORE NORMAL TISSUE PERFUSION
Blood pressure
Pulse
Respirations
Skin Appearance
Sensorium
Urine output (30-50 cc per hour)
Hemoglobin 8-10 gm or Hematocrit 24-30
Treatment
Secure, maintain airway
Apply high concentration oxygen
Assist ventilations as needed
Keep patient supine
Control obvious bleeding
Stabilize fractures
Prevent loss of body heat
Administer nothing by mouth, even if the patient complains of thirst
Treatment
Elevate lower extremities 8 to 12 inches in hypovolemic shock
Do NOT elevate the lower extremities in cardiogenic shock
Treatment
Surgery: immediate vs. delayed vs. none
Establish airway and deliver O2
Insert 2 large bore IVs
infuse Normal saline or Lactated Ringer’s
Treat mechanical causes of shock if they are present
Tension pneumothorax
Pericardial tamponade
Exsanguinating hemorrhage
Treatment
While inserting IVs, draw blood for laboratories and for blood typing
Relieve pain with IV narcotics
Reassess
Blood transfusion: think twice
Vasopressors
Antibiotics?
Treatment
Maintenance IV fluids
Inotropic support?
Early removal of septic focus (i.e. dead bowel or large abscess) or other definitive surgery
Blood transfusions
Good effects
Restores blood volume
Stays in vessels
Increases O2 delivery to tissues
Blood Transfusions
􀂇 Bad effects
􀂄 Transfusion reactions
􀂇 Febrile & allergic: 1/100
􀂇 Hemolytic
􀂃 Fatal: 1/100,000
􀂃 Non-fatal : 1/6000
􀂄 Transmission of disease
􀂇 Hep B: 1/200,000
􀂇 Hep C: 1/103,000
􀂇 HIV: 1/450,000
􀂇 Malaria, Chagas, Yersinia: < 1/1,000,000
􀂇 Overall 3/10,000
􀂄 Decreases immunity to cancer and infection
Hypovolaemic shock
control the bleeding
restore the victim's blood volume
Blood transfusions are necessary for loss of large amounts of blood (e.g. greater than 20% of blood volume)
Sodium is essential to keep the fluid infused in the extracellular and intravascular space whilst preventing water intoxication and brain swelling.
It is best treated by rapidly restoring intravascular volume and perfusion as above.
Inotropic and vasoconstrictive drugs -avoided, -interfere in knowing blood volume has returned to normal.
Regardless of the cause, the restoration of the circulating volume is priority.
As soon as the airway is maintained and oxygen administered the next step is to commence replacement of fluids via the intravenous route.
Opinion varies on the type of fluid used in shock. The most common are:
Crystalloids –
sodium chloride (0.9%),
Hartmann's solution (Ringer's lactate).
Dextrose solutions which contain free water are less effective at re-establishing circulating volume, and promote hyperglycaemia.
Colloids –
synthetic albumin (Dextran™),
polygeline (Haemaccel™),
succunylated gelatin (Gelofusine™)
hetastarch (Hepsan™). C
Colloids are, in general, much more expensive than crystalloid solutions and have not conclusively been shown to be of any benefit in the initial treatment of shock.
Combination –
can further exacerbate the problem and suggest the combination of crystalloid and colloid solutions.
Blood - Essential in severe haemorrhagic shock, often pre-warmed and rapidly infused.
Vasoconstrictor agents have no role -hemorrhagic shock,
due to their relative inefficacy in the setting of acidosis,
due to the fact that the body, in the setting of hemorrhagic shock, is in an endogenously catecholaminergic state.
Definitive care and control of the hemorrhage is absolutely necessary, and should not be delayed.
Cardiogenic shock
Inotropic agents, which enhance the heart's pumping capabilities, are used to improve the contractility and correct the hypotension.
Goals
re-establishment of circulation to the myocardium, minimising heart muscle damage
improving the heart's effectiveness as a pump.
performed by percutaneous coronary intervention and insertion of a stent in the culprit coronary lesion or sometimes by cardiac bypass.
The main way to avoid this deadly consequence is to make the blood pressure rise again with fluid replacement with intravenous infusions;
use of vasopressing drugs (e.g. to induce vasoconstriction);
anti-shock trousers that compress the legs and concentrate the blood in the vital organs (lungs, heart, brain).
blankets to keep the patient warm - metallic PET film emergency blankets are used to reflect the patient's body heat back to the patient.
Distributive shock
antibiotics
and supportive care is given (i.e. inotropicas, mechanical ventilation, renal function replacement).
Anaphylaxis
adrenaline to stimulate cardiac performance a
corticosteroids to reduce the inflammatory response.
Neurogenic shock
Trendelenburg position.
However, since blood vessels are highly compliant, and expand as result of the increased volume locally, this technique does not work.
More suitable would be the use of vasopressors.
Obstructive shock
obstructive shock
Pneumothorax or haemothorax is treated by inserting a chest tube,
pulmonary embolism requires thrombolysis (to reduce the size of the clot), or embolectomy (removal of the thrombus),
tamponade is treated by draining fluid from the pericardial space through pericardiocentesis.
Endocrine shock
hormone disturbances are corrected.
Hypothyroidism requires supplementation by means of levothyroxine,
Hyperthyroidism the production of hormone by the thyroid is inhibited through thyreostatica, i.e. methimazole (Tapazole®) or PTU (propylthiouracil).
Adrenal insufficiency is treated by supplementing corticosteroids.
Bleeding
Bleeding Significance
If uncontrolled, can cause shock and death
Identification of External Bleeding
Arterial Bleed
Bright red
Spurting
Venous Bleed
Dark red
Steady flow
Capillary Bleed
Dark red
Oozing
Control of External Bleeding
Direct Pressure
gloved hand
dressing/bandage
Elevation
Arterial pressure points
Splinting
Air splint
Pneumatic antishock garment
Control of External Bleeding
Tourniquets
Final resort when all else fails
Used for amputations
3-4” wide
write “TK” and time of application on forehead of patient
Notify other personnel
Tourniquets
Do not loosen or remove until definitive care is available
Do not cover with sheets, blankets, etc.
Epistaxis
Common problem
Incidence: 60.4/1000 ENT admitted patients.
M:F::2:1.
Most commonly involve age group of more than 60 years.
(JIOM 2006;28:2-4.)
Epistaxis
Management
Sit up, lean forward
Pinch nostrils together
Keep in sitting position
Keep quiet
Apply ice over nose
15 min adequate
Internal Bleeding
Can occur due to:
Trauma
Clotting disorders
Rupture of blood vessels
Fractures (injury to nearby vessels)
Internal Bleeding
Internal Bleeding
Signs and Symptoms
Pain, tenderness, swelling, discoloration at injury site
Bleeding from any body orifice
Internal Bleeding
Signs and Symptoms
Vomiting bright red blood or coffee ground material
Dark, tarry stools (melena)
Tender, rigid, or distended abdomen
Internal Bleeding
Management
Open airway
High concentration oxygen
Assist ventilations
Control external bleeding
Stabilize fractures
Transport rapidly to appropriate facility
Prognosis
Depends on the underlying cause and the nature and extent of concurrent problems.
Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy.
Septic shock however, is a grave condition and with a mortality rate between 30% and 50%.
The prognosis of cardiogenic shock is even worse.
Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in reinfused.
Perfusion of the brain may be the greatest danger during shock.
Urgent treatment (cessation of bleeding, rapid restoration of circulating blood volume and ready respiratory support) is essential for a good prognosis in hypovolemic shock.
Limitations
Failure to recognize occult hemorrhage
Do not assume hypotension after trauma is due to head injury.
Inadequate resuscitation
Remember points
Pediatric - Compensatory mechanisms may be quite effective in children. Hypotension is a late finding and represents significant hemorrhage.
Geriatric - Medications and underlying diseases may modify responses to cause or even therapy.
Pregnancy - Optimization of perfusion in the mother is the treatment of choice for the fetus.
