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pH less than 7.35 equals acidosis.

Look at HCO3 . If low, metablic acidosis is indicated; if high, may have mixed disorder or compensating response to respiratory acidosis.

Look at PCO 2 . If high, respiratory acidosis is indicated; if low, compensating for metabolic acidosis or a mixed picture is present.

pH greater than 7.45 equals alkalosis.

Look at HCO3 . If high, metabolic alkalosis is indicated; if low, may be compensating for respiratory alkalosis or a mixed picture is present.

Look at PCO 2 . If low, respiratory alkalosis is indicated; if high, may be compensatory for metabolic alkalosis or a mixed picture is present.

pH normal. Could be a mixed disorder or compensated disorder (or no disorder!). For example, if HCO3 - is low, and PCO 2 is high, either mixed respiratory acidosis and metabolic alkalosis or full

compensation of one for the other is indicated.

III Coagulation

A Mechanisms of hemostasis

Hemostasis can be divided into three phases.

Primary hemostasis

Platelet adherence: The first step in controlling hemorrhage is platelet adherence to the injured vessel. Glycoprotein receptor Ib in conjunction with von Willebrand factor mediates this step.

Platelet activation: Activated platelets produce thromboxane A 2 and other vasoconstrictors, which

reduce blood flow through the injured vessel. Glycoprotein IIb/IIIa is expressed, which promotes platelet-platelet adhesion (fibrinogen required) and formation of the platelet plug.

Clot formation. Tissue factor exposed due to vessel injury or in response to inflammation begins the clotting cascade. The cascade has traditionally been taught as having an intrinsic and extrinsic pathway; however, in vivo, both pathways act in concert. The extrinsic system usually begins the cascade with amplification by mechanisms of the intrinsic system. Components of the extrinsic system also activate the intrinsic system.

Extrinsic pathway: Tissue factor binds factor VII and activates it (VIIa). VIIa subsequently activates factor X. Xa then converts prothrombin to thrombin.

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Intrinsic pathway: In general, factor XIIa activates XI then Xia activates IX. IX then converges with the extrinsic pathway by activating factor X. This pathway can be initiated either by exposure to a negatively charged surface (exposed collagen from a damaged vessel) or thrombin itself activates factor IX.

Both pathways converge at factor X: Factor Xa then mediates activation of thombin with factor Va as a cofactor. Thrombin mediates fibronogen conversion to fibrin. Finally, factor XIIIa mediates cross linking of fibrin.

Regulation and fibrinolysis. The coagulation system is a cascade, meaning that each step in the process is a point of multiplication. Each activated intermediate factor is able to activate many of the factors in subsequent steps. Additionally, thrombin itself acts as a positive feedback loop by activating factor IX. The fibrinolyic system acts to keep the coagulation cascade under control and to remove clot once healing has started to occur.

Tissue factor pathway inhibitor (TFPI) may inhibit TF-VIIa complexes.

Protein C and protein S degrade factors V and VIII.

Antithrombin III inhibits thrombin-Xa complexes.

Fibronolysis: tissue -type plasminogen activator (t -PA) and urokinase -type plasminogen activator (uPA) mediate conversion of plasminogen to plasmin, which cleaves fibrin.

B Coagulopathy

A good history and physical should elucidate any problems with coagulation.

Lab studies should not be routinely ordered preoperatively in a patient with a negative history. Where the history is positive, studies can then be used to confirm and specify the diagnosis.

History

Include any perceived coagulopathy by the patient.

Bruising

Petechia

Easy bleeding/nosebleeds

History of unexplained bleeding from other procedures (dental/surgical)

Family history

Risk factors

Liver disease

Renal failure

Physical. Evidence of bruising, petechia, etc.

Lab evidence

Platelet count: Normal is 150,000–400,000/mL blood.

Keep >50,000/mL for general hemostasis.

<10,000/mL at risk for spontaneous bleeding.

>100,000 necessary if major surgery is being planned.

Bleeding time: measure of platelet function. Disorders of platelet function include:

Uremia

Drugs (aspirin, clopidogrel, gp IIa/IIB inhibitors)

von Willibrand's disease

Low count

Prothrombin time: measures extrinsic cascade. Since factors II (thrombin), VII, and X are produced by the liver, PT represents a good measure of vitamin K–dependent coagulation factors. It is therefore used to monitor warfarin therapy. The international normalized ratio (INR) is a normalization factor to equate lab values between labs.

Activated partial thromboplastin time (aPTT): measures intrinsic cascade. Useful for following patients on IV unfractionated heparin therapy.

Thrombin time: tests the conversion of fibrinogen to fibrin via thrombin. Is elevated when fibrinogen is depleted or nonfunctioning and in the presence of heparin.

C Specific hypocoagulopathic states

First, ensure bleeding is not a surgical complication. Do not necessarily blame postoperative bleeding on coagulopathy until surgical bleeding is ruled out.

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Liver disease: In severe liver disease, hepatocytes cannot manufacture clotting factors. PT/INR is elevated. Treatment includes replacing factors with fresh frozen plasma (FFP) or cryoprecipitate and medical management of the liver disease.

Renal disease: Uremia causes platelet dysfunction. Treatment can be with ddAVP, which causes release of von Willibrand's factor or FFP.

Disseminated intravascular coagulopathy (DIC): Microvascular coagulation due to inflammation from sepsis, trauma, and other severe insults leads to a consumption of factors. Lack of factors then leads to coagulopathy. The mainstay of treatment includes treating the underlying cause. Replacement of factors may exacerbate the condition, and paradoxically, anticoagulant therapy may be beneficial.

Consumption/dilution: due to severe trauma, sepsis, major surgery, and their attendant fluid resuscitation. Treatment involves correcting the underlying cause and replacing factors with FFP. Other mechanisms include hypothermia and acidosis in trauma patients, both of which inhibit proper clotting mechanisms.

Medically induced

Aspirin: permanently binds COX and prevents platelet aggregation.

Plavix: blocks ADP-mediated platelet aggregation.

Gp IIb/IIIA inhibitors: inhibit platelet aggregation.

Warfarin: blocks vitamin K–dependent liver synthesis of factors II, VII, IX, and X.

Heparin and heparinoids: augment antithrombin -III function.

The longer blood is stored, the worse it performs. Over time, cells lyse, and 2,3-DPG levels fall, causing oxygen to bind more avidly.

Febrile reactions/allergic: most common immune reaction. Usually related to either cytokines or donor leukocyte or other contaminants, or a mild antibody response. Usually self-limited. Can be prevented by leukodepletion and pretransfusion antipyretics.

Electrolyte disturbances

Hyperkalemia: Lysed cells can cause hyperkalemia.

Hypocalcemia: Citrate in stored blood can bind calcium.

Coagulapathy: pRBC's do not contain clotting factors or platelet. Large volume transfusion without these other products can cause a coagulopathy.

ABO incompatibility: Etiology is intravascular immune reaction, leading to clumping and lysis of red cells with mismatched blood. Signs and symptoms include hemoglobinuria, fever, chills, coagulopathy, renal failure, and circulatory collapse. Prevention is key by ensuring correct patient identity and blood type to avoid these preventable reactions.

ABO system: Patient's blood type is based on the ABO antigen system. Type A people make antibodies to B antigens, and type B to A. Type AB makes no ABO antibodies and hence is a universal recipient. Type O makes antibodies to A and B, and so these patients are universal donors (the cells have no ABO antigens), but they can receive only type O blood.

Delayed hemolytic reaction: Usually takes 3–7 days to manifest. Signs and symptoms include fever, malaise, hyperbilirubinemia, and decreasing hematocrit. Usually related to minor antibody systems such as the Rh system. Usually but not always preventable with recipient antibody screening. Treatment includes hydration and supportive care.

Rh system: A system of minor antigen -antibody that can cause reactions.

Disease transmission: Many virsues can be transmitted by blood. Prior to screening, this was a real risk. With modern screening methods such as nucleic acid technology screening, the risk is reduced but is not negligible.

HIV: Estimated to be 1:800,000.

Hepatitis C: Estimated to be 1:600,000.

Hepatitis B: Estimated to be 1:220,000.

Others: Risks less known but have been described. HTLV 1 and 2, West Nile virus, Creutzfeld-Jacob disease.

Immunosuppression: Probably the most significant but least thought of risks of blood transfusion. Negative outcomes include:

Morbidity in the form of increased infectious complications, including ventilator-associated pneumonia.

Possible increases in cancer recurrence following potentially curative surgery.

Increased mortality in intensive care unit (ICU) patients.

B Indications for transfusion

Given the negative effects of transfusions, who should be transfused ?

Prior transfusion triggers of a hemoglobin of 10 mg/dL or hematocrit of 30% were artificially set. Transfusion decisions should be based on individual patient circumstances. In general, it is safe to let the Hgb drop to 7 mg/dL and even lower in healthy, young individuals.

Cardiac patients: May need higher Hgb levels, but this is debatable.

Trauma patients: Exsanguinating patients should be given blood as resuscitation, as their Hgb is still high acutely, but they are losing blood and its attendant oxygen-carrying capacity.

Patients in class 3 hemorrhagic shock (1500 cc blood loss, signs of hypotension should be transfused empirically).

ICU patients: If needed, direct measurements of oxygen delivery and extraction can help to guide transfusion therapy.

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General patients: Only transfuse if symptomatic. Signs and symptoms from anemia can include tachycardia, tachypnea, and acidosis.

C Alternatives to transfusion

If the time of blood loss is known: elective surgery

Autologous banked blood

Epoetin alpha : Can increase the hematocrit preoperatively to help avoid transfusion.

Use of auto -transfusion technology: Recycle blood lost during surgery.

Acute normovolemic hemodilution: Once a patient is anesthetized, blood can be removed, stored, and replaced with crystalloid or colloid to maintain euvolemia. This has two benefits. Blood lost during surgery has a lower hematocrit, and therefore fewer red cells are shed. Those that are shed can be replaced with fresh (not stored) autologous blood.

Directed donor: risk of virus transmission lower, but similar risks of immunomodulation and other reactions

Hemostatic agents prevent blood loss in the first place!

FFP/cryoprecipitate for patients with coagulopathy.

DDAVP for patients with platelet dysfunction.

Aprotinin : inhibits serine proteases, including plasmin.

Lysine analogs: ε-aminocaproic acid.

Topical hemostatics: fibrin glue.

Acute unexpected blood loss

Autotransfusion may still be an option, if readily available.

Emergent aortic rupture

Trauma laparotomy

Quick prevention of further blood loss is the best therapy.

Chronic anemia

Accept a lower Hematocrit.

Epoetin alpha.

V Surgical Wounds and Wound Healing

A Classification of surgical wounds

Wounds are typically classified according to how the wound was made, how much contamination is present , and the expected rate of infection. There are four categories that determine if a wound should be closed or left opened and allowed to heal by secondary intention.

Clean wounds are incisions made under sterile conditions for a nontraumatic procedure that does not enter the bowel, tracheobronchial tree, genitourinary system, or the oropharynx and is not infected. A wound created to repair a hernia is an example of a clean wound. The infection rate for clean wounds should be less than 2%, and all clean wounds should be closed primarily.

Clean-contaminated wounds are similar to clean wounds, except that the bowel, tracheobronchial tree, genitourinary system, or the oropharynx was entered. There is minimal contamination of the wound, and the biliary, respiratory, and genitourinary tracts do not have any evidence of active infection. Routine cholecystectomy, colon resection, appendectomy, and bladder surgery are examples of the a cleancontaminated wound. The infection rate for clean-contaminated wounds should be 3%–4%, and these wounds are typically closed primarily unless other risk factors are present.

Contaminated wounds are similar to the clean and clean-contaminated wounds, except that there is major contamination of the wound during the performance of the procedure (e.g., gross spillage of stool from the colon; infection in the biliary, respiratory, or genitourinary system). Fresh traumatic wounds fall into this category. Examples of this type of wound are a bowel obstruction with enterotomy and spillage of contents and acute cholecystitis with pus in the gallbladder and spillage of pus. The infection rate for contaminated wounds should be 7%–10%, and these wounds are often left open.

Dirty and infected wounds occur when an established infection is present before a wound is made in the skin. Examples of this type of wound include an appendiceal abscess, traumatic

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wound with contaminated devitalized tissue, and perforated viscus. The infection rate for dirty wounds is 30%–40%, and these wounds should be left open.

B Normal wound-healing phases

The normal process of acute wound healing has sequential phases, eventually resulting in re-establishment of tensile strength. Depending on the extent of infection and hematoma present, this process can be delayed. Prolonged delayed healing for whatever reason can convert an acute wound into a chronic nonhealing wound.

Coagulation phase. Immediately following injury, the injured tissue and blood vessels release local

mediators intended to stop bleeding and begin healing. This results in vasoconstriction and increased permeability of local blood vessels, formation of fibrin, and platelet aggregation.

Inflammatory phase. The injured tissue of the wound develops an inflammatory response comprised of cellular, vascular, and mediator changes. In the absence of infection or other factors that delay wound healing, the inflammatory phase lasts approximately 1 week.

Cellular. The increased vascular permeability and chemokine release that occurs during the coagulation phases allows recruit and wound infiltration by polymorphonuclear cells (PMN). Activation and localization of PMN cells allows removal of necrotic tissue and debris, including invading microbes. After 24–48 hours, macrophages replace PMNs as the predominant inflammatory cells in the wound. Macrophages are necessary for remodeling of the extracellular matrix to facilate subsequent fibroblast migration and activity. Epithelial cell migration begins to occur, resulting in bridging across apposed tissue edges. Typically, by 48–72 hours, epithelial bridging and adherence across surgically closed wound edges has occurred.

Vascular. Disruption of blood vessels makes the wound area hypoxic. Hypoxia and the wound growth factors stimulate the growth of blood vessels (angiogenesis) from existing capillaries into the hypoxic area of the wound, making healing more effective. The initial hemostatic vasoconstriction converts to inflammatory vasodilitation, promoting fluid and mediator influx into the wounded region. These changes account for the localized erythema and edema associated with the wound.

Mediators. Injured cells, platelets, and recruited inflammatory cells release multiple mediators that promote wound remodeling and healing. Tissue growth factors such as transforming growth factor - beta and platelet-derived growth factor promote influx of fibroblasts. Chemokines and cytokines promote recruitment of additional inflammatory cells. Matrix metalloproteinases facilitate breakdown of injured tissue and remodeling of the wound.

Proliferative phase. As the inflammatory response in the wound subsides, fibroblasts that have migrated into the wound begin to form collagen, and wound strength begins to increase. Until collagen is synthesized in the wound, the strength of the wound is provided by the fibrin in the clot or scab. As myofibroblasts that have migrated into the wound multiply and begin to contract, the wound gets smaller. Wound contraction continues for several weeks or until the skin edges meet. Collagen production in the wound continues for approximately 3 weeks, then returns to the normal level.

Wound remodeling. Approximately 3 weeks after the injury occurred, the wound is essentially healed, and a scar is formed. During this period, the initial collagen that was synthesized during the proliferative phase in a haphazard way is degraded, and new collagen is synthesized and aligned along lines of stress. This newly directed collagen also has more cross links between collagen strands, which increases the strength of the scar. The scar tissue reaches approximately 90% of the original tissue strength in an average of 6 weeks; however, scar remodeling can continue for years.

C Acute wound care of surgical and nonsurgical wounds

Hemostasis must be obtained before wounds can be cleaned, debrided, and closed.

If adequate hemostasis is not obtained, a wound hematoma will develop. The presence of a wound hematoma extends the inflammatory phase of wound healing and increases the risk of wound infection. If the hematoma becomes infected, the inflammatory phase becomes more pronounced (i.e., all of the components of the inflammatory phase are increased), and healing is delayed.

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Hemostasis in most wounds can be obtained by direct pressure and by careful ligation of larger bleeding vessels. If hemostasis cannot be obtained by these methods because of congenital or acquired coagulopathy, the wound should be tightly packed until the coagulopathy can be controlled.

Cleansing

For optimum wound healing, all nonviable tissue, foreign bodies, and gross infection should be removed. The inflammatory phase is shortest with a clean, viable wound, which leads to the best strength and cosmetic result.

The first step is to remove all foreign material visible to the naked eye. In some instances, foreign material may be ground into the tissue (e.g., gravel in a motorcycle accident victim), and the tissue may need to be resected. Gross material can usually be removed with forceps, scalpels, or scrub brushes.

After foreign material is removed, nonviable tissue should be resected. Sharp debridement of grossly nonviable tissue is the most common approach. If tissue viability is questionable, then additional techniques such as IV fluorescein or tissue oxygen tension measurement can be utilized. These methods are cumbersome to perform during the acute care of a wound. A common and acceptable alternative is to not immediately debride the questionable tissue and to reinspect it in 24–48 hours.

After grossly visible foreign material and necrotic tissue have been removed, removal of microscopic debris and bacteria is beneficial. This is most commonly accomplished with 0.9% normal saline irrigation under pressure. Copious irrigation of the wound with nontoxic solutions reduces bacterial load without damaging underlying viable tissue. Use of betadine solutions, typically used for cleaning and disinfecting skin, should be avoided on open wounds because they can cause tissue damage and impede wound healing.

D Methods of wound closure

Primary closure. In wounds with a low risk for infection (i.e., clean wounds, clean-contaminated wounds, and minimally contaminated wounds), closure allows for the best result. In primary closure, the skin edges are approximated shortly after the wound is incurred, using any acceptable closure method.

Secondary intention. Wounds with a high risk for infection and wounds that are already infected are usually left open and allowed to heal by epithelialization and wound contraction. Epithelialization begins at the skin edges and concentrically progresses to the middle of the granulation bed. Infection and necrotic tissue will prevent granulation and wound epithelialization from occurring. Very large wounds can heal with good cosmetic results. Occasionally, wounds are too large for the epithelium to migrate over, and a skin graft is needed for final closure or to accelerate closure.

Delayed primary closure. Wounds that are heavily contaminated (e.g., perforated appendicitis) are likely to develop an infection if closed primarily, and therefore the skin should be left open. After 3–5 days, the wound may be primarily closed if no residual contamination is obvious. Good wound care and the body's natural defenses decrease the bacterial count sufficiently to allow closure during this time frame. However, if the wound is closed earlier or later, bacterial counts will be higher and sufficient to cause a wound infection.

Skin grafts. A skin graft is a split portion of the skin containing the epidermis and part of the dermis obtained from a normal skin donor site. Split -thickness skin grafts are used on well-granulating, noninfected, nonepithelialized superficial wounds to provide epithelial coverage for healing. Eventually, full incorporation including vascularization of the graft to the wound site occurs, allowing complete skin coverage. The thickness of these grafts is usually 15 microns but can vary from very thin (0.05 inch) to full - thickness epidermis and dermis. The thicker the graft, the more durable it is, and the less the wound contracts. However, the thicker the graft, the less frequently the donor site will heal or be able to be used again. As a result, very thick graft donor sites have more scarring and delayed healing, and there is less donor skin available for large wounds (e.g., a burn).

Flaps. Some wounds have underlying tissue loss in addition to skin loss and require replacement of this tissue for adequate return of function or cosmesis. These tissues require vascularization and must be transferred with their blood supply to survive.

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Rotation flap. The flap retains its normal blood supply but is mobilized to a different location to fill in a defect.

Free flap. The tissue is completely removed from its normal blood supply and is moved to another area of the body, where the blood vessels are reanastomosed to the local blood supply. This method allows tissues, such as a great toe, to be moved to the hand to replace a lost thumb.

E Wound dressings

Sutured wounds. It takes approximately 48 hours for the epithelium to migrate across a sutured wound and seal it. If there is no further drainage at that time, dressings are not needed except where necessary for patient comfort. Until the wound seals, it needs a dressing to absorb any drainage and to wick it away from the wound so that bacteria do not accumulate and multiply.

Open wounds

In the open wound that has necrotic debris , the purpose of the dressing is to help clean and debride the wound. The most common form of dressing for this type of wound is the wet -to -dry dressing. In this dressing, a thin piece of gauze is moistened, placed in the wound, and covered with dry dressing. The gauze is then allowed to dry. When the dry gauze is removed, it takes necrotic debris with it. The disadvantage of this type of dressing is that viable tissue is also removed, which slows wound healing.

A clean open wound or a dirty wound that has been cleaned by wet-to -dry dressings is most effectively treated with wet -to -wet dressings, in which the gauze is not allowed to dry. This keeps the tissues moist, does not debride healthy tissue, removes exudates, and enhances wound healing.

Large, open dermal wounds (e.g., skin graft donor sites) or large abrasions heal by epithelial migration and need a dressing that protects the underlying dermis and promotes epithelial migration. Dressings such as nonadhering petroleum -base impregnated gauze allow formation of a scab under the gauze, which facilitates epithelial migration. Nonpermeable dressings also can be applied to these wounds to keep the dermis moist and to allow epithelialization to occur faster.

F Factors that inhibit wound healing

Malnutrition. Malnutrition interferes with wound healing, and the more severe the malnutrition, the greater the deleterious impact on healing. In malnourished patients undergoing elective or urgent operation, a short course (10–14 days) of nutrition preoperatively improves wound healing. Nutritional support should be continued postoperatively in the malnourished patient. For the well-nourished patient undergoing surgery, nutritional support is not necessary for proper wound healing if normal nutrition will resume within 5–7 days. Preoperative albumin is the best guide to the risk of malnutrition -related wound healing impairment.

Diabetes. Hyperglycemia inhibits virtually all aspects of the body's inflammatory response and immune system, which leads to increased susceptibility to infection and decreased wound strength. If the patient's glucose is well controlled (80–120 mg/dL), the wound healing should be virtually normal. Therefore, aggressive control of blood glucose during the perioperative period is essential. These patients may require frequent blood glucose determinations and a constant insulin infusion.

Jaundice. Jaundice has been associated with inhibiting normal wound healing. This may be due either to the hyperbilirubinemia or the underlying liver dysfunction causing jaundice and other hepatic-related