Shock and Wound Healing - labsstudies

Shock and Wound Healing

Shock and Wound Healing

Shock

• A clinical syndrome caused by a critical reduction in blood flow within the microcirculation, resulting in insufficient tissue perfusion and oxygen delivery to meet the nutritional needs of cells and the removal of metabolic waste products.

 Causes of Shock

Shock can be caused by a number of mechanisms, including:

  •  Low circulating plasma volume.
  • Failure of the heart to eject an adequate amount of blood.
  •  Poor venous return from any cause.

Types of Shock

  •  Cardogenic shock
  •  Hypovolaemic/haemorrhagic shock
  • Septic shock
  • Anaphylactic shock
  •  Neurogenic shock

Cardiogenic Shock

  • Inability to pump enough blood to supply all body parts.
  • This is acute circulatory failure with a sudden drop in cardiac output but no actual reduction in blood volume (normovolemic shock).

Cardiogenic shock can be caused by:

  •  A heart attack, heart failure, or cardiomyopathy.
  • Valvular heart disease (VHD)
  •  Cardiac arrhythmias

Hypovolaemic/Haemorrhagic Shock

  •  Loss of blood or fluids to the outside or into tissues (shock can be caused by internal (concealed) or external (revealed) haemorrhage.
  •  Internal haemorrhage can be concealed, as in a ruptured spleen or liver, fractured femur, ruptured ectopic pregnancy, or cerebral haemorrhage.
  •  External haemorrhage is a concealed haemorrhage that becomes visible, such as hematemesis or melena from a bleeding peptic ulcer or hematuria from a ruptured kidney, and it can also be caused by severe burns.

Septic shock

  • Is a serious condition that occurs when a severe infection/septicaemia causes low blood pressure and low blood flow
  •  Toxins damage vessel walls, causing them to leak and become unable to contract well.
  • This most commonly occurs in the setting of gram-negative Bacteria (endotoxic shock), but it can also occur in the setting of gram-positive and fungal infections..
  •  Causes vessel dilation, resulting in hypovolaemia.

Anaphylactic shock

  • A widespread immunoglobulin E hypersensitivity reaction to a specific antigen causes vasodilation and increased vascular permeability, Resulting in decreased perfusion and impaired cellular metabolism.

Cause of anaphylactic shock include:

  •  Insect bites/stings, horse serum (used in some vaccines), food allergies, and drug allergies are all causes of anaphylactic shock.

Neurogenic shock

  •  Shock caused by insufficient peripheral resistance as a result of widespread vasodilation.

Common causes include:

  •  Spinal cord damage
  •  Injuries to the central nervous system
  •  Excruciating pain

The Pathophysiology and Sequelae of Shock

Pathophysiology

  • There is systemic hypoperfusion (inadequate blood supply to cells and tissues) due to a decrease in cardiac output or a decrease in effective circulating blood volume, resulting in an inadequate supply of oxygen and nutrients to distal tissues.

Sequelae

  •  A decrease in effective circulating blood volume causes hypotension, impaired tissue perfusion, cellular hypoxia (tissue hypoxia/anoxia), and if not compensated for impaired cellular metabolism and death of the patient.

Shock Stages

Reversible Shock

  •  Also known as initial or compensated shock.
  •  It occurs in the early stages when an attempt is made to maintain adequate cerebral and coronary blood supply by redistributing blood supply to vital organs (brain, heart, and kidney) so that they are well oxygenated.

 Compensatory mechanisms include:

  •  Increased heart rate o constriction of peripheral blood vessels
  •  Dilatation of coronary and cerebral vessels
  •  Stimulation of the rennin, angiotensin, and aldosterone axis.

Irreversible Shock

  •  At this stage, the shock is so severe that there is no recovery despite compensatory mechanisms, therapy, and control of the aetiologic agent causing the shock.
  •  There is a progressive drop in blood pressure due to low cardiac output caused by a myocardial depressive factor (MDF).
  •  Impaired circulation exacerbates the condition by failing to adequately remove the end products of cell metabolism.
  •  Endothelial damage increases vessel permeability, exacerbating hypotension.
  •  This causes severe metabolic acidosis due to anaerobic glycolysis, respiratory distress (adult respiratory distress syndrome-ARDS) due to pulmonary oedema, and ischaemic cell death of end organs.

 

Wound Healing

  • It is a complex and dynamic process of restoring cellular structures and tissue layers.
  • The wound healing process can be divided into three distinct phases:
  • Inflammatory phase
  •  Proliferative phase
  •  Remodeling phase
  •  Within these three broad phases is a complex and coordinated series of events that includes chemotaxis, phagocytosis, granulation, collagen degradation, and collagen remodeling.
  • Furthermore, angiogenesis, epithelialization, and the production of new glycosaminoglycans and proteoglycans are critical to wound healing.

 

Types of Wound Healing
There are three types of wound healing, include:

 Primary wound healing

  • This is also referred to as healing by first intention.
  • When the wound’s edges are in aposition, this occurs within hours of repairing a full-thickness surgical incision.

Delayed primary wound healing

  •  Occurs if the wound edges are not immediately reapplied.
  • By the fourth day, phagocytosis of contaminated tissues has begun, and epithelialisation, collagen deposition, and maturation have begun.
  •  Foreign materials are walled off by macrophages, which may metamorphose into epithelioid cells, which are surrounded by mononuclear leukocytes and form granulomas.
  •  Chronic inflammation may occur, resulting in visible scarring.

 Secondary healing

  •  This is also known as secondary intention healing.
  •  Secondary wound healing causes a more intense inflammatory response than primary wound healing.
  •  Additionally, due to the need for wound closure, a greater quantity of granulomatous tissue is produced.

 Events in Wound Healing

  • After tissue injury, a cascade of vasoconstriction and coagulation begins, with clotted blood immediately impregnating the wound and leading to hemostasis.
  • An influx of inflammatory cells occurs, resulting in the release of cellular substances and mediators
  • Angiogenesis and re-epithelialization occur, and new cellular and extracellular components are deposited.

 The wound healing event sequence includes the following phases:

Initial phase (Hemostasis)

  • Following vasoconstriction, platelets adhere to damaged endothelium, discharge adenosine diphosphate, promoting thrombocyte clumping and damming the wound.

Second phase (Inflammation)

  •  In the second phase (inflammation), polymorphonuclear leukocytes (PMNs) engulf the wound.

Third phase (Granulation)

  • This phase is divided into four subphases: fibroplasia, matrix deposition, angiogenesis, and re-epithelialization.

Fourth phase (Remodelling)

  •   The wound changes constantly, which can last for years after the initial injury.

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