The Body's Reaction to Surgical Treatment and Injuries

Introduction to Surgical Injury

• Surgery as Injury: Surgery is fundamentally a form of injury to the body. This is true whether the injury is accidental or intentional (surgical intervention).

• Scope of Response: Following an injury, characteristic changes occur categorized into two types:

  • Local changes: Occurring at the specific site of tissue damage.

  • Generalized changes: Affecting the entire body systemically.

• Recovery Objective: The primary purpose of these physiological processes is to facilitate recovery and restore the body to its pre-injury state.

• Proportionality and Modifiers: The intensity of the metabolic reaction is generally directly proportional to the severity and extent of tissue damage. However, this reaction can be modified by external or secondary factors, most notably infection.

Pathophysiology of Local Tissue Damage

• Macrophage Activity ($\text{aktywacja makrofagów}$):

  • Engagement in phagocytosis ($\text{fagocytoza}$).

  • Release of biochemical mediators including cytokines ($\text{cytokiny}$), eicosanoids ($\text{eikozanoidy}$), and proteases ($\text{proteazy}$).

• Neutrophil (Granulocyte) Response ($\text{gromadzenie się granulocytów obojętnochłopnych}$):

  • Accumulation at the site of damage.

  • Phagocytosis and the further release of cytokines and proteases.

• Endothelial and Vascular Events:

  • Infiltration: Neutrophils adhere to endothelial cells, followed by migration into the damaged tissues.

  • Barriers breached: Bacterial invasion ($\text{inwazja bakterii}$) and bleeding into tissues ($\text{krwawienie do uszkodzonych tkanek}$).

  • Afferent Signaling: Stimulation of afferent impulses ($\text{pobudzanie impulsacji aferentnej}$) to alert the Central Nervous System.

• Biochemical Activation Cascades ($\text{uczynnienie osoczowych kaskad aktywacji}$):

  • Coagulation system ($\text{krzepnięcie}$) and blood platelets ($\text{płytki krwi}$).

  • Activation of the Complement system ($\text{dopełniacz}$).

• Endothelial Activation ($\text{aktywacja śródbłonka}$) and Edema:

  • Massive leakage of fluid and proteins into the tissue space ($\text{przeciekanie płynu i białek}$).

  • Development of tissue edema ($\text{obrzęk tkanki}$).

  • Capillary dilation ($\text{rozszerzenie naczyń włosowatych}$).

  • Significant increase in capillary permeability ($\text{wzrost przepuszczalności włośniczek}$).

Leukocyte Infiltration and Molecular Signaling

• Chemokine Triggering: Injury to tissues and vessels triggers the immediate release of specific chemokines, such as:

  • $CCL2$

  • $CXCL10$

  • $SEMA3A$

• Signaling and Angiogenesis:

  • Proangiogenic Factors: Includes $HIF-1\alpha$, $VEGF$, $ANG1$, and $IL-8$.

  • Cell Interactions: Direct interaction between macrophages and Endothelial Cells ($EC$). Macrophages are responsible for guiding tip cell sprouting and fusion during tissue repair.

  • $M2$ Polarization: Driven by signaling networks such as the $Notch$ signaling pathway.

• Cellular Components Involved: Monocytes, Neutrophils, $M1$ macrophages, $M2$ macrophages, and Smooth Muscle Cells ($SMC$).

Systemic Hypovolemia and the "Third Space"

• Definition: Hypovolemia is a reduction in circulating blood volume, which is a hallmark result of moderate to severe injuries.

• Primary Etiologies:

  • Direct loss of body fluids: This includes blood, stomach contents, sweat, vomiting, and simple water loss.

  • Fluid Sequestration: Retention of plasma-like fluid in damaged tissues, technically referred to as the "third space." This is caused by increased endothelial permeability throughout the body.

• Clinical Consequences:

  • Reduction in total circulating blood volume.

  • Resultant reduction in the total volume of oxygen delivered to tissues.

  • Significant slowing of the healing process.

  • Accumulation of secondary tissue damage due to ischemia.

Hormonal and Metabolic Preservation Mechanisms

• Fluid Saving Mechanisms: The body activates specific endocrine pathways to conserve fluids through various glands.

• Pituitary Gland ($\text{przysadka mózgowa}$) secretions:

  • Growth Hormone ($GH$).

  • Adrenocorticotropic Hormone ($ACTH$).

  • Prolactin.

  • Aduretic Hormone (also known as Antidiuretic Hormone, $ADH$).

• Adrenal Glands ($\text{nadnercza}$) secretions:

  • Adrenaline ($\text{adrenalina}$).

  • Cortisol ($\text{kortyzol}$).

  • Aldosterone ($\text{aldosteron}$).

• Pancreas ($\text{trzustka}$):

  • Glucagon ($\text{glukagon}$).

• Renal Influence: The activation of the Renin-Angiotensin system.

• Metabolic Shifts:

  • Maintenance of blood flow prioritized.

  • Acceleration of overall metabolism and energy consumption.

  • Transition into states of catabolism and starvation to meet energy demands.

Systemic Effects of Surgery and Injury by Organ System

• Fever and CNS: The Thalamus/Hypothalamus ($\text{wzgórze}$) triggers fever ($\text{gorączka}$).

• Cardiovascular System ($\text{układ krążenia}$):

  • Increased sympathetic tension ($\text{napięcia współczulnego}$).

  • Pronounced acceleration of heart rate (Tachycardia).

• Hepatic Metabolism ($\text{wątroba}$):

  • Increased glycogenolysis ($\uparrow \text{glikogenolizy}$).

  • Increased gluconeogenesis ($\uparrow \text{glukoneogenezy}$).

  • Increased lipolysis ($\uparrow \text{lipolizy}$).

  • Increased production of ketone bodies ($\uparrow \text{produkcji ciał ketonowych}$).

  • Increased synthesis of acute-phase proteins ($\uparrow \text{syntezy białek ostrej fazy}$).

• Renal System ($\text{nerki}$):

  • Activation of the Renin-Angiotensin-Aldosterone System ($RAAS$).

  • Increased reabsorption of $Na^+$ and $K^+$ ions.

  • Decreased total urine volume ($\downarrow \text{objętości moczu}$).

  • Notably weak erythropoietin response to trauma-induced anemia.

• Musculoskeletal and Bone Marrow:

  • Skeletal Muscles ($\text{mięśnie szkieletowe}$): Increased muscle breakdown ($\uparrow \text{rozpadu mięśni}$) and the release of amino acids into the bloodstream.

  • Bone Marrow ($\text{szpik kostny}$): Disturbances in the formation of red blood cells.

• Site-Specific Reactivity:

  • Inflammation ($\text{zapalenie}$), edema ($\text{obrzęk}$), and endothelial activation at the operative site.

  • Increased local blood flow and stimulation of afferent nerves.

Perioperative Fluid and Electrolyte Management

• Nutritional/Hydration Limitations: Surgical patients are typically unable to drink during anesthesia preparation or post-surgery. Prolonged intake limitations necessitate intravenous ($IV$) fluid replacement.

• Monitoring Requirements: Water and electrolyte balance are influenced by the patient's daily medications. Careful perioperative monitoring of fluid balance is essential.

• Chronic Fluid Loss: Long-term losses, such as those from fistulas, require meticulous accounting for electrolyte depletion reaching beyond simple water replacement.

Composition of Common Blood-Substitute Fluids

• 5% Glucose: Includes no electrolytes; $pH$ value is approximately $4.0$.

• 0.9% NaCl (Normal Saline):

  • $Na^+$: $154\,mmol/dm^3$

  • $Cl^-$: $154\,mmol/dm^3$

  • $pH$: $5.0$

• Ringer's Lactate (Hartmann's Solution):

  • $Na^+$: $131\,mmol/dm^3$

  • $K^+$: $5\,mmol/dm^3$

  • $Cl^-$: $112\,mmol/dm^3$

  • $HCO_3^-$: Equivalent to $29\,mmol/dm^3$ (converted from lactate in the liver).

  • Included ions: $Ca^{2+}$ ($1\,mmol/dm^3$) and $Mg^{2+}$ ($1\,mmol/dm^3$).

  • $pH$: $6.5$

• Haemaccel (Succinated Gelatin):

  • $Na^+$: $145\,mmol/dm^3$; $K^+$: $5.1\,mmol/dm^3$; $Cl^-$: $145\,mmol/dm^3$; $Ca^{2+}$: $6.25\,mmol/dm^3$.

  • Oncotic Pressure: $370\,mm\,H_2O$.

  • Plasma Half-life: $5\,\text{hours}$.

  • $pH$: $7.4$

• Gelofusine (Polygelated Gelatin):

  • $Na^+$: $154\,mmol/dm^3$; $K^+$: $0.4\,mmol/dm^3$; $Cl^-$: $125\,mmol/dm^3$; $Ca^{2+}$: $0.4\,mmol/dm^3$; $Mg^{2+}$: $0.4\,mmol/dm^3$.

  • Oncotic Pressure: $465\,mm\,H_2O$.

  • Plasma Half-life: $4\,\text{hours}$.

  • $pH$: $7.4$

• Hydroxyethyl Starch (Skrobia hydroksyetylowana):

  • $Na^+$: $154\,mmol/dm^3$; $Cl^-$: $154\,mmol/dm^3$.

  • Oncotic Pressure: $310\,mm\,H_2O$.

  • Plasma Half-life: $17\,\text{days}$.

  • $pH$: $5.5$

• Human Albumin 4.5%:

  • $Na^+$: $150\,mmol/dm^3$; $Cl^-$: $120\,mmol/dm^3$.

  • Oncotic Pressure: $275\,mm\,H_2O$.

  • $pH$: $7.4$

Acid-Base Balance and Clinical Disorders

• Disorder Classification: There are four basic types: Metabolic Acidosis, Respiratory Acidosis, Metabolic Alkalosis, and Respiratory Alkalosis. These can occur in isolated or mixed forms.

• Diagnostic Basis: Measurement involves arterial blood gas ($ABG$) analysis and lactate concentration levels.

• Metabolic Acidosis:

  • Characterized by increased hydrogen ion ($H^+$) concentration and decreased plasma bicarbonate ($HCO_3^-$) levels.

  • Compensation: Respiratory system compensates by hyperventilating to lower $PaCO_2$ below normal.

• Metabolic Alkalosis:

  • Characterized by decreased $H^+$ and increased $HCO_3^-$ concentration.

  • Comorbidities: Usually accompanied by Hypokalemia and Hypochloremia.

  • Main Cause: Loss of chlorides.

• Respiratory Acidosis:

  • Frequency: Often occurs in the postoperative period.

  • Characterized by an increase in $PaCO_2$, $H^+$, and $HCO_3^-$ ions.

Respiratory Alkalosis: Etiology and Gasometry

• Pathophysiology: Excessive excretion of $CO_2$ due to lung hyperventilation.

• Clinical Causes:

  • Pain.

  • Hyperventilation associated with hysteria.

  • Pneumonia ($\text{zapalenie płuc}$).

  • CNS Disorders: Meningitis ($\text{zapalenie opon mózgowo-rdzeniowych}$) and encephalopathy ($\text{encefalopatia}$).

  • Pulmonary embolism ($\text{zator tętnicy płucnej}$).

  • Sepsis.

  • Salicylate poisoning.

  • Liver failure ($\text{niewydolność wątroby}$).

• Acute Uncompensated Gasometry Results:

  • $H^+$: Decreased (resulting in increased $pH$).

  • $PaCO_2$: Decreased.

  • Actual $HCO_3^-$: Normal or decreased.

  • Standard $HCO_3^-$: Normal.

• Metabolically Compensated Gasometry Results:

  • $H^+$: Normal (full compensation) or slightly increased (partial compensation).

  • $PaCO_2$: Decreased.

  • Actual and Standard $HCO_3^-$: Decreased.

Definition and Classification of Shock

• Definition: Shock represents a critical imbalance between oxygen supply and demand. This leads to cellular dysfunction, cell death, organ failure, and systemic death.

• Types of Shock:

  • Cardiogenic shock.

  • Hypovolemic shock.

  • Neurogenic shock.

  • Anaphylactic shock.