DOCTOR-PATIENT RELATIONSHIP

Interaction that is established between a doctor and patient with the goal of restoring health, alleviate suffering, and preventing disease The doctor needs to establish a dialogue with the patient that plays a

significant role in the success of therapy, as well as to apply theoretical and technical knowledge for DX & TX

There is a dialogue of the relevant medical procedures Also need to remember the family members, because the suffering can either

bring a family together or tear them apart Respect for the patient consists of reciprocity, communication, and concern

It is not shown in the “informed consent” but in the sensitive and attentive response to the nuances of patient behavior, both verbal and non-verbal

The doctor-patient relationship It is not only professional, but humane It displays the dignity of each party

Dignity is an emotional need of having public recognition by authority, personal, friends, family, social circles of having done things well It is an intrinsic quality of being human It is based on the recognition that the person is worthy of respect

It is developed in the hope of curing and being cured It needs empathy, trust, compassion, and sensitivity It is unequal in professional terms, but not in human terms The characteristics of the doctor needed to maintain a doctor-patient

relationship: Knowledge Wisdom Humanity Empathy Willingness to help when facing difficulties

Types of relationships Active-passive

Is provided for patients w/ a coma or if the patient is in a state where active participation is not possible

Guided cooperation Is established w/ patients that are in a condition where they can

cooperate with the doctor in their DX & TX, such as in some acute & chronic diseases such as pneumonia or arterial HTN

Mutual participation Not only compliance w/ TX, but the patient is actively participating in

the discussion of situations and attitudes related with the cause & evolution of the disease

In reality, seeing the patient as a client and the use of modern technology in medical practice has increased errors in the practice of medicine, violating the principles of medical ethics & facilitating the participation of lawyers in malpractice claims The dilemma of the specialist: they know more about the disease, but

understand less of being humane

Rights of the patient To receive adequate medical attention for their state of health and the

specific circumstances of their case, and to be informed when there is a need for references of any other doctor

To be treated w/ trust and that their health information is not divulged to those not expressively authorized

To be treated in a dignified & respectful manner. The doctor, nurses, and all personnel must identify themselves and respect at all times the patients personal and moral convictions

Have the option to obtain a second opinion on DX, TX, or PX To receive information that is sufficient, clear, timely, and accurate of DX,

PX, and TX To receive medical care in case of emergency at any health establishment,

whether public or private To be able to decide on the type of care without any form of pressure, as

well as to accept or reject each diagnostic procedure offered and the person performing the procedure

To have a clinical record w/ information that is truthful, clear, accurate, legible, and complete

Stress and surgery The response to all stressful stimuli, real or symbolic, is a complete

response of the individual, integrated at all levels, from the molecular level and the psychologic level, to the biochemical modifications and changes in behavior

The surgical procedure has many symbolic meanings, different for each operation and for each patient

The surgical procedure is a brutal assault, adding to the aggression of the disease itself, as it consists of pain, danger of death, violation of the body itself by a stranger, mutilation, and of transitory state of death with no guarantee of the brevity

Why is a good doctor-patient relationship important? b/c with it, you can arrive at a more precise DX for the disease b/c we will be able to motivate the patient to the extent possible b/c the patient and the family will be better able to appreciate our work b/c it is important to develop a good clinical history, a document that is

essential in the scientific and legal aspect How to have empathy for a patient? SMILING IS FREE

By first greeting the patient and encouraging them to introduce us to their problem

By being quiet during the interrogation By smiling and exhibiting the ability to listen with sincerity By talking when you need, and giving explanations about their condition By maintaining orderly records SMILING DOESN’T CURE, BUT ALLEVIATES. PRESENCE IS NOT

ENOUGH, BUT IS GRATIFYING

PREOPERATIVE EVALUATION

Integral determination of state of health of a patient that will be submitted for surgery, with the goal of identifying diseases that can affect the prognosis, the surgery itself, or the recuperation from surgery Objective

To evaluate surgical patients to determine if it is necessary to implement therapeutic measures (prophylaxis) so that the patient can tolerate the surgery without any major problems

To reduce Perioperative morbidity and mortality Requirements

Definition of actual physiological state of the patient To determine all pathological processes and their grade of activity Evaluation of nutritional status To delineate physical, cognitive, and emotional state To identify the surgical risk factors (pre/trans/post-operative) Plan of action to minimize risks

Advantages Evaluation of anesthetic risk

ASA 1 = healthy patient, w/o physical/metabolic abnormalities 2 = patient w/ mild-moderate deterioration of physical state

that does not interfere w/ their daily activities 3 = patient w/ severe metabolic/physical disorders that

interfere w/ daily activities 4 = patient w/ severe life-threatening disorders 5 = moribund patient w/ limited life-expectancy w/in the next

24 hours Preparation of surgery includes recommendation for fasting & any

indication for pre-medication Prevention of possible complications Treatment of existing pathologies Formulation of anesthetic plan Obtainment of informed consent

Document which establishes communication from the doctor to the patient informing them of the surgical process that is to come, the alternative options, potential complications, risks and benefits, that the patient accepts with their signature

Separate authorization for: Blood transfusions Anesthesia & its risks

Risks Respiratory

Pulmonary dysfunction It is important to evaluate respiratory function in patients w/

pulmonary problems in case they deteriorate, which represents a major risk of presenting w/ complications such as atelectasis, hypoxia, and pneumonia postoperatively

Risk factors Intense smoker

Cough Obesity Advanced age Intra-thoracic operations Pre-existing lung disease

Risk I = normal Risk II = chronic smoker, controlled chronic pulmonary

disease, acceptable VC & respiratory volume Risk III = chronic smoker, controlled chronic pulmonary

disease, acceptable VC & respiratory volume, limited pulmonary function tests

Risk IV = Acute or active chronic pulmonary disease, w/ poor pulmonary function, hypoxia, hypercapnia

Pulmonary thromboembolism Low risk = TX w/ compressive measures Moderate risk = TX w/ compressive measures, low-dose

heparin (5000 U tid or bid) High risk = TX w/ compressive measures, heparin, or LMWH,

or warfarin Cardiovascular

Based on: Risk I = normal patient Risk II = patient older than 40 or less than 40 & arrhythmic, or w/

previous heart surgery, or hypertensive, or MI more than 6 months ago

Risk III = patient older than 40 or less than 40 & arrhythmic, or w/ previous heart surgery, or hypertensive, MI more than 6 months ago, or with history of infarct less than 6 months ago

Risk IV = decompensated cardiac function, need to evaluate for risk in arterial & venous system studies

Goldman Cardiac Risk Index S3 = 11 Elevated JVP = 11 MI in past 6 months = 10 ECG: premature arterial contractions or arrhythmia = 7 ECG shows > 5 premature ventricular contractions/min = 7 Age > 70 = 5 Emergency procedure = 4 Intra-thoracic, intra-abdominal, or aortic surgery = 3 Poor general or metabolic status, bedridden = 3 Severe aortic stenosis = 3

Patients w/ scores > 25 had a 56% incidence of death, w/ a 22% incidence of severe CV complications

Patients w/ scores < 26 had a 4% incidence of death w/ a 17% incidence of severe CV complications

Patients w/ scores < 6 had a 0.2% incidence of death w/ a 0.7% incidence of severe CV complications

Hepatic

The patient w/ hepatic disease constitutes a challenge for the medical team in perioperative management, and the determination of potential surgical risk is proportional to the severity of hepatic compromise Must evaluate immunologic, metabolic, and circulatory function of

the liver Hepatic surgery risk

I = normal II = Group A of Child classification

Albumin > 3.5 g/L Bilirubin < 2 mg/dL (w/ cholestasis, < 4) PT% > 50% or INR < 1.7 Ascites absent No encephalopathy

III = Group B of Child classification Albumin 2.8-3.5 g/L Bilirubin 2-3 mg/dL (4-10) PT% 30-50% or INR 1.8-2.3 Mild ascites Grade 1 or 2 encephalopathy

IV = Group C of Child classification, in case of acute disease evaluation of LFT Albumin < 2.8 g/L Bilirubin > 3 mg/dL (>10) PT% < 30% or INR > 2.3 Moderate ascites Grade 3 or 4 encephalopathy

Renal Renal surgery risk

I = normal evaluation II = slightly elevated BUN & creatinine, creatinine clearance of 40-

60 ml/min III = creatinine clearance of 20-40 ml/min IV = creatinine clearance < 20 ml/min or patient on dialysis

Hematologic Hematologic surgery risk

I = normal II = Hb & Hct up to 20% less than normal value, slightly elevated

coagulation factors III = Hb & Hct b/w 20-40% less than normal, altered coagulation

factors, thrombocytopenia, active hematologic disease IV = Hb & Hct more than 40% less than normal, w/ severely

affected coagulation factors Endocrine-metabolic

Endocrine-metabolic surgery risk I = normal II = slightly decompensated (diabetic w/ hypoglycemia) III = decompensated (insulin-dependent) IV = severely decompensated (decompensated diabetic)

Neuro-psychiatric Neuropsychiatric surgery risk

I = normal II = GCS 11-13, controlled neurologic disease, anxiety, depression III = GCS 9-11, psychiatric problems in TX IV = GCS < 9, schizophrenia, psychosis

Glasgow Coma Scale Open eyes

None = 1 To painful stimuli = 2 To vocal command = 3 Spontaneously = 4

Best verbal response None = 1 Incomprehensible sounds = 2 Utters inappropriate words = 3 Confused, disoriented = 4 Oriented, converses normally = 5

Best motor response None = 1 Extension to painful stimuli = 2 Abnormal flexion to painful stimuli = 3 Flexion/withdrawal to painful stimuli = 4 Localizes painful stimuli = 5 Obeys commands = 6

Nutritional Nutritional surgery risk

I = normal II = loss of 10% of body weight w/ hypoproteinemia w/o

associated diseases III = loss of 20% of body weight w/ hypoproteinemia, associated to

chronic disease, albumin 2-2.5 mg/dL IV = loss of > 20% of body weight w/ hypoproteinemia, associated

to chronic disease, albumin < 2 mg/dL Infection & sepsis

Surgical risk I = normal II = patient w/ chronic controlled process III = acute infectious process, septic syndrome IV = septic shock

Age Surgical risk

18-40, 41-60, 61-80, >81 Condition of surgical intervention

Risk I = elective II = urgent III = very urgent

IV = immediate or life/death Initial evaluation form

ID & profile of patient Type of condition

Acute, acquired, localized, complicated w/ … Manifested by: synopsis of clinical case Acknowledgement of following syndromes (list in order of severity) Acknowledgement of primary cause & any complications

Proposal of DX studies Lab Imaging

Proposal of following management Immediate TX Mediate TX Post-mediate TX Late TX

Preoperative evaluation General measures

Informed consent Fasting Bed position Vital signs (SVPT) Nursing general care (CGE) Obtain IV access Elastic measures (anti-thrombotic prophylaxis)

Parenteral solutions Begin or continue w/ previously indicated plan

Reset solutions Maintenance solutions

Medications Continue w/ medications already initiated

Abx Anaglesics, KCL

Add Omeprazole 40 mg c/24 hours Enoxaparin 20 mg c/ 12 hours SC

Special measures Supplemental O2 (nasal points 4-5 L) Vigilance of tubes (NG, urinary, catheters) Note entry and exit of balance of liquids every 12 hours Solicit CXR, interconsult w/ cardio, w/ anesthesiologist Justification of indications Pass to operating room at 7 AM

Transoperative evaluation Anesthesia Anti-sepsis of operating region Technique of preparation of operating field Technique of laparotomy

Description of surgical technique Technique of closure of laparotomy

Postoperative evaluation Recuperation: ICU, hospital bed

General measures Position Mobilization of bed O2 Vital signs every 15 min General nursing care

Parenteral solutions Mixed solution 1 L for 4 hours NaCl 1 L for 4 hours Dextrose 5% 1 L for 8 hours + 2 ampules of KCL

Medications Ketorolac or Meperidine every 4-6 hours Continue Abx, enoxaparin, omeprazole

Special measures O2 nasal Monitor functioning of tubes & catheters Change of position & exercise every 4-6 hours Form of balance of liquids Removal of NG tube when hear intestinal sounds Initiate PO De-ambulation in 12-36 hours Discharge the following day w/ appointment to remove sutures in 8

days

PERIOPERATIVE ANALGESIA Pain

Characteristics of postoperative pain Nociceptive Involve inflammatory mediators such as:

Prostaglandins Histamine Serotonin Bradykinin

Involves A delta fibers Is acute, w/ variable intensity

30% of recently operated patients suffer from intense pain 40% of recently operated patients suffer from moderate pain 20% of recently operated patients suffer from mild pain

Objective of perioperative analgesia Decrease the stress response, which fundamentally consists of a

neurovegetative response manifested by: Elevation of BP, HR, CO Greater oxygen consumption (organic respiration to surgical stress)

Avoid hyper-excitability of neurons of dorsal horn, by a single dose of

preoperative analgesia Permit “normal” activity of patient, with supplemental analgesics Decrease hospital stay and costs Decrease postoperative complications

Thrombosis d/t delayed de-ambulation Pulmonary alterations d/t retention of secretions or hypoventilation Atelectasis Eschar Thromboembolism Muscular contraction d/t pain

International Association for the Study of Pain (IASP) Recommendations NSAIDs for parenteral use in acute pain

Antipyretic analgesics Propacetamol ampoule of 1-2g IV qid Metamizol ampoule of 2g IV/IM tid/qid Ketorolaco ampoule of 30mg IV/SC/IM qid

Potent analgesic, but w/ moderate anti-inflammatory activity w/ similar analgesic & anti-inflammatory actions to other

NSAIDs, but 350 times more potent than aspirin Inhibits platelet aggregation & can damage gastric mucosa Administration (PO, IV, IM, SC, rectal): the max plasma

concentration can be achieved in 30-60 min, w/ max effects in 2 hours, and lasts 6 hours

It is partially metabolized in the liver & excreted in the urine Renal elimination is prolonged in renal insufficiency & elderly Efficacy

30mg of ketorolac IM = 100mg of meperidine IM (12 mg of morphine IM)

Dosage Ketorolac 30mg qid (no more than 120mg/d for 5 days IV)

In elderly above 65, 15mg qid (no more than 60mg/d for 5 days IV)

Anti-inflammatory analgesics Ketoprofeno ampoule of 100mg IV tid Diclofenaco ampoule of 75mg IM bid Dipirona 1g IV slow infusion (max 4g/d) repeated tid/qid

Opioid analgesics Tramadol 100mg diluted in 100ml physiologic fluid passed in 10

minutes, repeated qid (max 400mg/d) Dextropropoxifeno 38mg/dipirona 1g in 100ml physiologic fluid,

repeated tid (max 152mg/4g/day) Morfina

Full agonist of receptors mu, delta, and kappa Fundamental activity on mu receptors Absorbed via all routes except transdermal Excreted via urine (half-life of 2-4 hours)

Epidural analgesia Most used epidural analgesics are local anesthetics (bupivacaine,

ropivacaine, and lidocaine) and opioids Opioid (fentanyl)

Duration of action is relatively short w/ lipophilic character (prevents the incidence of late respiratory depression associated with epidural morphine)

Most probable side effect of fentanyl is pruritis, which responds normally to a decrease in dose or antihistamines

Can resemble sedation, especially in the elderly, that only respond to a decrease in velocity of perfusion or to removal of medication

Other possible secondary effects are nausea, delay of intestinal motility, and occurrence of distended bladder

Protocol of epidural analgesia w/ PCA pump 200ml saline + 200mg bupivacaine + 600microg fentanyl at 5-

10 ml/hour w/ bolus of 1 ml 200ml of 0.2% ropivacaine + 600microg fentanyl at 5-10

ml/hour w/ bolus of 1 ml Examples of perioperative analgesia

Infiltration of wound: at the end of surgery, a local anesthetic of long duration (0.25% bupivacaine)

Peribulbar or retrobulbar block for ocular surgery or topical analgesics In children, regional anesthesia before surgery reduces the

requirements of general anesthesia w/ subsequent lower incidence of N/V and early & high tolerance

Patterns of treatment Once the surgery is completed, the patient is moved to recuperation

Pain is controlled = initiate IV analgesic protocol Pain is not controlled

Mild pain = NSAID Metamizol 2g Ketorolaco 30mg Propacetamol 2g

Moderate pain = NSAID + Tramadol 50mg + Metoclopramida 10mg in 100cc saline

Severe pain = potent opiate Meperidine 25mg every 4-6 hours until pain is controlled Morphine 2-5mg & later 1mg until pain is controlled

COMPLICATIONS IN SURGERY Any divergence from the predicted course in the systemic recuperation of

operated patient Are the result of the primary disease, the surgical intervention, and other

non-related factors For early detection, it is necessary to repeatedly evaluate the patient Prevention of complications begins before surgery

Important factors in postoperative stage Early mobilization

Adequate respiratory care Liquid and electrolyte balance

Classification Anatomical area

Neurologic Respiratory Cardiovascular Digestive Renal

Extension of anatomical area Local Systemic

Time of presentation Immediate (first phase): w/in OR & up to recuperation area

Anesthetic induction-beginning of surgery Dysrhythmias HR alterations Cardiac arrest Bleeding Defective hemostasis

During the time of surgery Prolongation of estimated operative time Change in route of access Shock state Transfusions

w/ conclusion of surgery-anesthetic reversion Sutures Installation of drainage systems Equipment for immobilization Late recuperation of alert state

Odontologic (loss of dental pieces) Ocular (conjunctivitis, corneal lesions) Musculoskeletal (lumbalgia, pharyngitis, laryngitis, phlebitis) Dehiscence of wounds, rupture of sutures, N/V, headache

Recent (second phase): in bed or intensive therapy Respiratory

Dyspnea Respiratory insufficiency Pulmonary infection Pulmonary thromboembolism Pneumonia Pneumothorax Atelectasis

Cardiovascular Tachycardia Arrhythmias Shock HF

Phlebitis DVT

Neurologic Disorientation Loss of consciousness Headache

Renal Renal insufficiency Oliguria Hydroelectrolytic disequilibrium

Late (third phase): w/ discharge and until full recovery Headache Pulmonary infections Respiratory insufficiency Phlebitis DVT Depression GI dysfunction Hepatic insufficiency Renal insufficiency Eschar Anemia Muscular weakness Myalgia Anorexia

Probability of presentation Avoidable vs inevitable Predictable vs unpredictable

Complications of surgical wounds Evaluate health status of patient Anti-sepsis of operative area, as well as adequate hemostasis Prophylactic antibiotic therapy

Seroma Accumulation of ECF

Separates layers of skin Cuts numerous lymphatic vessels

TX Drain by puncture Tetracycline 1g in 150ml saline Re-intervention to ligate lymphatics

Hematoma Accumulation of blood & clots Frequent, imperfect hemostasis

Pain Increase in local temperature Swelling Ecchymoses

If small, drain w/ open puncture & give prophylactic Abx

Keloids Excessive accumulation of collagen tissue in response to trauma TX

Extirpation w/ or w/o graft Partial resection Radiotherapy Local steroids (triamcinolone)

Dehiscence of wounds Partial or total rupture of any of the layers of a wound

5% in older than 60 M > F On postoperative day 5-8

Etiology Infection Poor surgical technique Poor selection of suture material Anemia, DM, uremia, malnutrition, cirrhosis Deficient tissue perfusion

3 important risk factors Inadequate closure: use of insufficient amount of sutures or placement

too close to the border Increase in intra-abdominal pressure: obesity, cirrhosis, cough Deficient curing of wound d/t seroma, hematoma

Evisceration Exposure of abdominal contents outside the limits of the parietal

peritoneum Increase in intra-abdominal pressure Dehiscence of surgical wound

Syndrome of abdominal compartmentalization Cellulitis

Inflammatory process d/t bacterial infection which extends via skin or subcutaneous tissue Edema Redness Heat/hyperthermia Headache

Local measures Cold compression Local cleaning Topical Abx

Systemic measures Abx therapy Synthetic & selective

Necrotizing fascitis Local

Erythema Distant tumefaction Distant cellulitis

Absence of crepitus Systemic

Toxemia Mental apathy Dehydration Negative cultures

Associated w/ DM, Immunosuppression TX

Ample debridement Systemic Abx therapy

Gaseous gangrene Rare, is produced by anaerobic bacteria Is related to the type of surgery Clinical presentation

Intense pain at wound 12-72 hours postoperatively Hyperthemia (39.5-41) Tachycardia (120-140) Grayish pallor Severe shock Subcutaneous crepitus Alterations in consciousness Diaphoresis

TX Debridement of wound Abx Hyperbaric oxygen therapy Amputation

MC systemic complications in surgery S/S

Fever = atelectasis/infections/post-transfusion/drugs/thrombophlebitis Tachycardia & anxiety = hypovolemia Dyspnea = hypoxemia, arrhythmias, sepsis, pain Hypotension = hypovolemia, sepsis, HF, anaphylaxis, bleeding Oliguria = hypovolemia, ARF

MANAGEMENT OF BURN PATIENTS Burns

Lesions in skin d/t physical (temperature), chemical, electrical, and radiational over-exposure Differ in severity, extension, and depth of affected tissue

Superficial (epidermal) Dress w/ tulle gras and gauze if extensive until healed (usually

w/in 1 week) Superficial partial thickness

Dress w/ tulle gras and gauze & re-assess at 48 hours Heal w/in 2-3 weeks

Low exudate May be suitable for Hypafix, wash dressing daily

and take off with oil in 1 week High exudate

If contaminated or signs of infection, apply antimicrobials & need to refer

If not contaminated, continue w/ tulle gras or Bactigras and review every 2 days until healed

If not healed w/in 2-3 weeks Requires surgery (refer to burn unit)

Deep partial thickness Obvious deep dermal injury

Requires surgery, preferably w/in 5 days, unless < 1cm2 in area

If no obvious deep dermal injury Dress w/ tulle gras and gauze, reassess at 48 hours

Signs of improvement in healing Re-dress and review every 2 days

If unhealed at 2 weeks, requires surgery & refer to burn unit

If no signs of improvement in healing If unhealed at 2 weeks, requires surgery & refer to

burn unit Management

Airway: compromised or at risk of compromise? Yes = intubate No = BREATHING

Breathing: compromised? Yes = cause

Mechanical: escharotomies CarboxyHb: intubate & ventilate Smoke inhalation: nebulizers, ventilation Blunt injury: invasive ventilation, chest drain

CIRCULATION Circulation: compromised perfusion to an extremity?

Yes = escharotomies No = NEUROLOGICAL DISABILITY

Neurologic disability: impaired GCS score? Yes = consider hypoxia or hypovolemia No = EXPOSURE

Exposure: fully assess burn areas & depth, full examination of concomitant injuries, keep warm

Fluids: calculate resuscitation formula based on surface area & time since burn

Heat burns Cutaneous cellular damage caused by increase in temperature at the cellular

level T < 45 = w/o evident damage T = 45-50 = diverse grades of lesion T > 50 = evident cellular damage w/ presence of denaturation of

cellular proteins Skin

0.25 sq m in children (up to 1.8 sq m in adults) Epidermis

Stratum corneum Stratum lucidum Stratum granulosum Stratum spinosum Stratum basale

Dermis Formed by fibroconnective tissue Amorphous in the region of blood vessels Nervous plexus 2 layers

Papillary dermis Reticular dermis

Hypodermis Subcutaneous tissue

Etiology Multiple causes

MCC Direct flame Hot liquids Direct contact w/ hot metals Electric current

Other causes Chemical (acidic/alkali) Spark Atomic radiation

Extension of burn Should be quantified while taking into account the extent of the burn Rule of 9 (in children)

Head = 9 (18) Anterior thorax = 9 Anterior abdomen = 9 Right superior extremity = 9 Left superior extremity = 9 Right inferior extremity = 18 (14) Left inferior extremity = 18 (14) Genitals = 1

Rule of palm Adults = palm of the hand including fingers = 1% of total surface

area Children = palm of hand including fingers = 2% of total surface

area Classification

Depth First degree = epidermis

Painful erythema Intact basal membrane Management

Healthy in 5-7 days spontaneously apart from basal layer Only require application of moisturizer In case of important discomfort (burning), prescribe an

analgesic Second degree

Superficial Erythema Presence of ampoules Underlying tissue is white w/ pressure Is painful Management

Debridement of ampoules Cleaning w/ water & soap everyday is there is no NaCl Apply sterile dressing Healthy in 3-4 weeks Generally do not require reconstructive procedures

Deep More pallor Can be gray or opaque Hypoesthetic

Third degree Extensive destruction of skin Painless lesions Coffee-colored or black lesions Dry, hard, w/ no elasticity No vesicles No sensitivity Management

In burn unit Always require reconstruction First, only apply sterile dressing

Immediate IV fluid therapy Burn of airways

Symptoms: can cause swelling that blocks airflow Charred mouth Burned lips Burns on head, face, or neck Wheezing Change in voice Difficulty breathing, coughing Singed nose hairs or eyebrows Dark, carbon-stained mucus

Incidence of burns Mortality & frequency of burns

Scalding = 22% (mortality of 10%)

Inflammatory liquids = 16% (6%) Explosions = 11% (13%) Burning homes = 5% (44%)

Causes of burns in children Scalding = 42% Inflammatory liquids = 10% Oils = 7%

Sites of burns Forearm Hand/wrist Arm Face

Special burns Chemical burns

Acids = cause denaturation of cellular proteins Alkali = cause caseation of cellular proteins Management

Immediate removal of whatever is causing damage Apply continuous irrigation (running water) for 1-2 hours (2-4

hours for alkali burns) Do not apply neutralizing agents

If burns for phosphorus, lithium, or sodium, no water Electric burns

Low-voltage < 1000 V High-voltage > 1000 V Non-evident lesions Can cause arrhythmias At least, maintain medical observation for 24 hours, w/ ECG every 8

hours & continual monitoring Management

Definitive management of burns Apply graft

Partial thickness Complete thickness

Fluid therapy Restoration of liquids when possible Begin application of formulas when the burnt surface is at least 20% or

if lesions are of second/third degree Remember that fist degree burns do not require restoration of liquids Formulas

Evans Brooke Parkland

First 24 hours: Hartman (Ringer’s lactate) 4ml/kg/%SA burnt of second/third degree Half in the first 8 hours Quarter in the next 8 hours Quarter in the next 8 hours

Diuresis of 30-70 ml/h Second 24 hours

Dextrose 5% in water to conserve Na at 140 mEq/L Colloid solution (plasma) to conserve blood volume in

patients w/ burns of second/third degree affecting more than 40% of total body surface area

Diuresis of 30-100 ml/h Hypertonic (Monafo) Half Carbajal

First 24 hours Ringer’s lactate: 5000ml/sq m burnt in adults

2000ml/sq m burnt in children Colloid: 12.5g/L of Ringer’s lactate

Second & third 24 hours Ringer’s lactate: 2500ml/sq m burnt in adults

2000ml/sq m burnt in children Colloid: 12.5g/L of Ringer’s lactate

Escharectomy Cut skin to free the tension of eschar When there is vascular compromise distally or w/ respiration Performed in ER

Factors for hospitalization Burns of > 10% of total body surface area in patients under 10 & over 50 Burns of > 20% of total body surface area in patients b/w 10-50 Burns of third degree greater than 5% in any age Pre-existing medical disorders Extremes of life Chemical burns Inhalation lesions Presence of other major trauma Burns of special areas

Control of pain Meperidine 25-50mg infusion every 2-4 hours Morphine sulfate 2.5-5.0mg IV Hydromorphine chlorhydrate 0.5-1.0mg IV repeated every 2-4 hours Antihistamine

TX A,B,C Initiate fluid therapy w/ strict control of liquids Realization of ambulatory surgical process in case it is needed Complete evaluation & transfer to burn unit Debridement & excision of necrotic tissue

Autografts Grafts: mallados Flaps Cultivated skin Heterografts & allografts

Synthetic substitute for skin (Integra) Split skin graft donor site management

Split-thickness skin grafting is recommended for third & fourth degree burns

Involves harvesting skin from an unaffected part of the patient (epidermis & superficial dermis) Donor sites heal in 10-14 days but can be very uncomfortable Potential for complications

Extreme discomfort Intense pain Leakage of blood Serous fluid & infection

Traditional dressing w/ open-weave tulle impregnated w/ petroleum jelly, covered by an absorbent layer of gauze & cotton wool

Goals Promote rapid wound healing Reduce pain Provide a barrier to infection Absorb copious amounts of exudate Be easy to handle & apply Be removable w/o traumatizing the new epidermis Not impede the morality of the patient No antigenic or allergenic Reduce the risk of hypertrophic scarring Inexpensive & accessible

Dressings Tulle gras: tulle adheres firmly to raw surface until healing is

complete Silver sulfadiazine: Abx cream that is effective in reducing risk of

infection Calcium alginates: promote blood clotting & wound healing by

creating a moist environment Film dressings Biological dressings

Topical antibiotics Silver sulfadiazine Sodium mafenide Platinum nitrate of 0.5% Iodopolivinilpirrolidona (isodyne)

Complications of burn patients Cardiovascular

Hypovolemic shock Acute MI HTN Myocarditis

Respiratory Inhalation wound

Pneumonia Acute respiratory insufficiency Pulmonary edema

Renal Renal insufficiency Myoglobinuria

GI Curling ulcers Hepatic dysfunction Alithiasic cholecystitis

Metabolic & nutritional Lack of nutrition Prolonged catabolism

Endocrine Suprarenal bleeding Insulin/glucagon disequilibrium

Neurologic Burn encephalopathy w/ carbon monoxide intoxication

ACID-BASE DYSEQUILIBRIUM The respiratory apparatus have sensitive chemoreceptors in the concentration of

H+ in the CNS, in the aorta, and in the bifurcation of the carotids The principal function of the cardio-respiratory function is supplying the

cells of the body with the blood flow to enable to be viable in ideal conditions

The kidney participates in the maintenance of acid-base equilibrium via: Regulates urinary excretion of circulating bicarbonate Excretes hydrogen ions

The most important buffer is sodium bicarbonate which reacts w/ carbonic acid Other substances that act as significant buffers are Hb, other proteins,

phosphates, and carbonates Arterial blood gases (ABG)

Evaluate the state of acid-base equilibrium (used preferentially in peripheral venous blood)

Evaluate hemodynamic state, using venous saturation of oxygen in central venous blood

Essential applications The evaluation of diffusion of gases at the pulmonary & systemic level The evaluation of the relation b/w acids & bases of ECF

pH Measures the global results of acid-base equilibrium It is not a parameter of evaluation of respiratory function Time of respiratory alteration If a respiratory process is acute or chronic, or when a chronic process

becomes acute PaCO2

Measures partial pressure of CO2 in arterial blood Is a parameter that is related to respiration

PaO2 Measures the partial pressure of oxygen in arterial blood Is a parameter which uses oxygenation in respiration

HCO3 Measures basic component of acid-base equilibrium Acute or chronic process

Anion gap To maintain electroneutrality

Positive load (cations) must equal negative load (anions) If not, normal anion gap is 8-16 mEq/L calculated by:

Na – Cl – HCO3 Metabolic acidosis

When HCO3 decreases, pH decreases = acidosis The body tends to increase the level of ventilation (hyperventilation) and

the CO2 decreases pH < 7.35 HCO3 < 22 mEq/L PaCO2 < 35 mmHg (if there is compensation)

Uncompensated metabolic acidosis (compensated) pH < 7.23 (7.32) PaCO2 = 35 mmHg (< 27 mmHg) HCO3 < 19.2 mEq/L (< 13 mEq/L)

Etiology Loss of bicarbonate d/t diarrhea Excessive production of organic acids d/t hepatic diseases a/o

endocrine alterations Shock Intoxications d/t drugs (salicylates) Inadequate excretion of acids d/t renal insufficiency Parenteral nutrition

S/S Rapid & deep breathing Fruity breath Hypotension Ventricular arrhythmias N/V Deterioration of level of consciousness, headache, confusion, & coma

TX Correct the cause of acidosis Correct the input of deficit of bases (input of bicarbonate if pH < 7.2)

Complications Hypovolemic shock, septic shock Hyperchloremia Deficiency of insulin High-output diarrhea Terminal phase of renal failure Fistula (pancreatic, duodenal, ileal) Non-adaptive ileostomy

Metabolic alkalosis If bicarbonate increases & produces an increases of pH, and is produced by

an increases in bases or HCO3 The body produces hypoventilation by increasing the level of CO2

pH > 7.45 HCO3 > 26 mEq/L PaCO2 > 45 mmHg (if there is compensation)

Etiology Loss of acids d/t prolonged vomiting or gastric aspiration Loss of K+ by increase in renal excretion (w/ diuretics) Alkaline antacids

S/S Slow & shallow breathing Muscular hypertonia Restlessness Fasciculations Confusion Irritability Coma

TX Administration of NaCl or KCl depends on the severity of

hypokalemia, before cases of severe or persistent alkalosis can require NH4Cl

Complications Hyperchloremic

Loss of chloride Gastric aspiration Vomiting Cerebral edema

Respiratory acidosis When bicarbonate increases, pH decreases The organism increases bases, eliminates acidic urine by the kidney,

pH < 7.35 HCO3 > 26 mEq/L (if there is compensation) PaCO2 > 45 mmHg

Uncompensated respiratory acidosis (compensated) pH < 7.22 (7.36) PaCO2 > 70 mmHg HCO3 > 27.4 mEq/L

Etiology CNS depression d/t drugs, lesions, or illness Asphyxia Hypoventilation d/t pulmonary disease, cardiac disease,

musculoskeletal disease, or neuromuscular disease S/S

Diaphoresis Headache Tachycardia

Confusion Nervousness

TX Treat the disease Mechanical ventilation in severe forms a/o accompanied by hypoxemia Assisted ventilation before a chronic hypercapnia is indicated only if

there is an acute increase in PCO2 Respiratory alkalosis

If the bicarbonate decreases & CO2 also decreases d/t hyperventilation, there is an increase in pH

pH > 7.45 HCO3 < 22 mEq/L (if there is compensation) PaCO2 < 35 mmHg Etiology

Hyperventilation for pain, anxiety, or inadequate use of ventilator Respiratory stimulation for drugs, asthma, hypoxia, fever Hepatic insufficiency Exercise

Uncompensated respiratory alkalosis (compensated) pH > 7.53 (7.38) PaCO2 < 23 mmHg HCO3 < 18.7 mEq/L (< 14.2 mEq/L)

S/S Rapid and deep breathing Paresthesia Anxiety Fasciculations

TX First treat the cause Then treat the hyperventilation w/ sedatives or have the patient breathe

into a brown paper bag Complications

Sepsis Pneumonia Thoracic trauma Pain Hyperthermia Anxiety Tachycardia Hepatic failure Mechanical ventilation

ABG Renal compensatory conditions or primary respiratory situations, are slow

to be evident w/in 48 hours, however respiratory compensation to metabolic abnormalities subsequent to primary metabolic alterations are done in a matter of minutes, given the large volume of CO2 that is managed by the lungs in the short term

Acidosis

Alteration of electrical status of multiple proteins Enzymatic systems fail Hyperkalemia Hyperchloremia Alterations in state of consciousness Muscular weakness Failure of cardiac rhythm

Coronary & cerebral vasodilation Pulmonary vasoconstriction Decrease in RV pressure Myocardial depression

Alkalosis Tetany (reduction of Ca++ ions) Hypokalemia (entry of K+ into ICF) Coronary & cerebral vasoconstriction Pulmonary vasodilation Diaphragmatic depression Hypokalemia & Hypochloremia

Surgery Acid-base disorders most frequent in surgical patients is metabolic acidosis Non-lethal acid-base disorders in surgical patients are metabolic alkalosis

& respiratory alkalosis

ORGANIC RESPONSE TO SEVERE LESION Response to lesion

Set of organizational changes that occur during the process of convalescence following an organic lesion. In what is lost in the acute form, the local & systemic homeostasis, and

the favorable circumstances, permitting anatomical, functional, and psychic re-establishment: Physiologic field

Series of events aimed at restoring homeostasis & repairing the tissue damage as quickly as possible

Courses w/ a self-immune response, but do not develop SIRS Express clinically the presence of generalized systemic

endothelial inflammation, independent of the productive cause

3 or more of the following conditions Temperature > 38 or < 36 HR > 90/min Respiratory rate > 20/min or PaCO2 < 32 WBC > 12000 or < 4000 or 10% bands

w/ a duration of 5-10 days from surgery, ADH & aldosterone levels returned to normal & to recover and a tenth of cortisol recuperates its circadian rhythm of secretion

Pathophysiologic field Set of events, beyond the horizon of their physiological

development & lead to the extremes of the body:

Immunologic dissonance Hypercatabolic state Cardio-circulatory instability

Consisting of all previous events that decimate the functional reserve, to the extent that the response itself becomes a threat to life

Etiology of acute & deep loss of homeostasis Severe accidental lesion

Multiple trauma Severe burns

Extensive elective lesions Transplants Surgical TX of cancer Surgical control of abdominal sepsis Orthopedic surgery of extremities under ischemia Hip surgery Colon surgery Cardiac surgery w/ extra-corporeal pump

Severe disease Shock Sepsis Organic failure: renal, hepatic, intestinal Acute respiratory failure

Pneumonia Severe asthma Acute pulmonary edema Decompensated COPD

Severe disease Extensive tissue infarct Severe intoxications Systemic vasculitis Cancer in advanced stages DKA Severe pancreatitis AIDS

Triggers therapeutics Blood-derived transfusions Idiosyncratic & drug response

Anaphylaxis Malignant hyperthermia Epidermal necrolysis

Immunotherapy, chemotherapy, a/o radiotherapy Prolonged transoperative hypotension Alveolar recruitment Thrombolysis (follows w/ ischemia-reperfusion)

Metabolic response to trauma Ebb phase

Defend homeostasis (perfusion volumes, pH)

3-24 hours Decreased balance of N2 Diminished tissue perfusion Cold, clammy skin Slow capillary filling Diminished central temperature

Flux phase Lesion has priority: mobilization of protein stores

1-14 days Catabolic phase Increased metabolic load Decreased balance of N2

Lesion & body have priority: reconstitution of protein stores Weeks Anabolic phase Increased balance of N2

High cardiac output Hypermetabolism Increased energy output Accentuated protein catabolism

Pathophysiology of the problem (sepsis) The monocyte-macrophage system is being stimulated by bacteria or its

products, and secretes inflammatory mediators or pro-inflammatory cytokines including TNF, IL1, IL2, IL6, IL8 Simultaneous secretion of anti-inflammatory cytokines such as IL4,

IL10, w/ the goal of modulating of action of pro-inflammatory cytokines

Monocytes release an inflammatory response Pro-inflammatory = SIRS = death Balanced response = resolution Anti-inflammatory = CARS = death

Apoptosis & necrobiosis The type of cellular death determines immunologic function of

surviving cells (CD4 T cells) Apoptotic cells: induce anergy or presence of anti-inflammatory

cytokines & block the immune response: auxillary Th2 cells & IL4 & IL10

Necrotic cells: Induce an inflammatory state creating an immune response & incrementing antimicrobial defenses: Th1

Neuroendocrine response Physiologic

Retain Na & water for guaranteeing circulating volume Maintain catabolism of macromolecules that provide substrates for

synthesis of energy, conservation of acid-base state Modulate the immunologic response, maintenance of epithelial barriers

& reparation of sites of lesion Nutrition

Set of interconnected factors to achieve:

Homeostasis Energy Growth Restoration of organism

The nutrition of human organism, depends on cellular metabolism which consists of 2 fundamental phases Anabolism

Biosynthesis of macromolecules To grow & maintain structure (proteins) For caloric-energy reserve (glycogen, lipids)

Catabolism Oxidation of nutrients for the production of energy (AcCoA + O2 =

ATP) and the elimination of waste products (CO2, NH2) Nutrition in fasting & stress (trauma, surgery, sepsis)

The stimulus of the neural & endocrine systems block the adaptation & establish a hypercatabolism, which in these situations is proportional to the magnitude of stress Greater requirement for glucose, fat, and protein for muscle repair

of injured tissues The effects of catabolic hormones will be reflected in the

proteolysis Increments of Basal Energy Needs following type of stress:

Elective surgery: 10-25% Trauma: 10-30% Sepsis: 50-80% Burns: 100-200%

Complications of malnutrition Delay of scarring Depression of immunocompetence Decrease in resistance to infection Sepsis Death

CV response Physiologic

Adequate flow & perfusion pressure to organic demand Its ability to generate pressure produces interstitial fluid continually w/

continual flow, carrying oxygen & energetic substrates of cells Transporters & mediators leads to the elimination of substances

Intravascular volume depletion and hypotension Generalized or localized reduction in renal blood flow = ischemic ARF

GI, renal, and dermal losses: hemorrhage, shock Large vessel renal vascular disease

Renal artery thrombosis/embolism, operative arterial cross-clamping, renal artery stenosis

Small vessel renal vascular disease Vasculitis Atheroembolism HUS

Malignant hypertension Scleroderma Preeclampsia Sickle cell anemia Hypercalcemia Transplant rejection

Sepsis Hepatorenal syndrome Medications

Cyclosporine Tacrolimus ACE inhibitors NSAIDs Radioconstrast agents Amphotericin B

Decreased effective intravascular volume CHF HF Cirrhosis Nephrosis Peritonitis

Immunoendothelial response At the local level, limits the damage, destroys infecting agents, removes

dead tissue, and limits necrosis & apoptosis Promotes local hemostasis & tissue repair At the systemic level protects the body against invasive pathogens

Pathophysiology (in sepsis) Bacterial aggression, triggers a series of immunologic responses to

combat the aggression that also causes damage to the body Vascular endothelium

Rolling mediated by selectins PMN: L-selectin Endothelium: P/E-selectin

Firm adhesion mediated by integrins PMN: LFA-1, Mac-1 Endothelium: ICAM-1, VCAM-1

Transmigration PECAM, VLA-4

Identification of organic dysfunction like markers of severe sepsis Altered consciousness, confusion, psychosis Tachypnea

PaO2 < 70 mmHg SaO2 < 90% PaO2/FiO2 < 300

Icterus Positive enzymes

Decreased albumin Increased PT

Tachycardia Hypotension Decreased central venous pressure

Oliguria/anuria Increased creatinine

Decreased platelets Increased PT Decreased protein C Increased D-dimers

LIQUIDS & ELECTROLYTES Homeostasis is maintained by coordinated action of hormonal adaptations

TBW (50-75%) of body mass, and changes w/ sex, age, & fat content In newborns, 75-77% In children 1-12 months, 65.5% In children 1-10 years, 61.7% In adults, b/w 50-60% of body mass In relation to sex, in adolescence, there is a greater water content in

males d/t the higher fat content in women ICF represents 40% of mass ECF represents 20% of mass Plasma constitutes 5% of mass Interstitium constitutes 15% of mass Transcellular fluid (lymph, peritoneal, pericardial, pleural, CSF) 1-2%

Regulation of body water Regulation of entry & excretion Thirst, which is regulated by the medial hypothalamic center, is a major

defense against depletion of liquid & hypertonicity Kidneys: RAS & ADH Excretion of body water is regulated by a variation in the rhythm of

urinary flow ADH or vasopressin

Controls reabsorption of water in renal tubules Regulates hydroelectrolytic balance of body fluids Increases cellular permeability in distal tubules & in collecting

ducts Decrease formation of urine

Sufficient kidney is a major ally to a patient undergoing inadequate management of liquids & electrolytes The kidney is the effector organ in the response to loss of

hydroelectrolytic homeostasis The kidney makes fine adjustments on the volume of body water &

electrolyte concentration Effective circulating volume

The proportion of circulating volume that inhibits compensatory response of homeostatic receptors

Entry Liquids: 1200 ml

Food: 1000 ml Metabolic: 350 ml

Loss Urine: 1500 ml Passive loss: 900 ml Sweat 50 ml Feces 100 ml

Electrolytes Cations in body water include Na, K, Ca, Mg

Na+ Excreted via the kidneys & via skin by sweating Excreted in great quantities when body temperature is high, during

exercise, fever, or emotional tension Hyponatremia < 135 mEq/L

Causes Pseudo-hyponatremia induced by active osmotic molecules

(glucose, mannose, glycine) Provoke a displacement of water, w/o altering the

quantity of sodium, which decreases the concentration (dilutional hyponatremia)

An increase of 100 g/dL glucose provokes a decrease in 1.7 mEq/L of Na

Pseudo-hyponatremia induced by active non-osmotic molecules (TG, proteins) These molecules reduce the relative % of water in a

determined volume of plasma Elevation of 1 g/dL of TG decreases natremia by 1.7

mEq/L Elevation of 1 g/dL of plasma proteins cuases a

decrease in natremia of 1 mEq/L Loss of Na

Renal Diuretics Osmotic diuretics Hypoaldosteronism Nephropathy w/ salt loss Diuresis Postobstructive

Digestive Vomiting Drainage tube Fistulas Obstruction Diarrheas

Cutaneous Sweating Burns

Drugs

Physical exercise CNS alterations: hemorrhage, astrocytomas,

hypopituitarism S/S

GI: N/V Peripheral nervous system: muscle tremors, visual

alterations CNS: lethargy, convulsions, coma

TX Hyponatremia w/ diminished ECF

Administration of isotonic saline solutions Na = (140 mEq/L – Na actual) x (0.6 x weight)

Hyponatremia w/ minimally increased ECF Initial TX is based on restriction of fluids In the presence of neurologic symptoms, administer

hypertonic saline solution (20%) along w/ small doses of loop diuretics (furosemide)

For more severe cases, administer urea at 10-30% which provokes osmotic diuresis

Hyponatremia w/ increased ECF Characterized by the presence of edema, and is related

with HF, nephrotic syndrome, and cirrhosis TX is based on restriction of liquids & salt along w/

administration of loop diuretics Hypernatremia > 150 mEq/L

Pathophysiology Insufficient action of ADH

Deficit of central production Loss of renal response

Excessive loss of water Renal Extra-renal

Positive salt balance Iatrogenic Primary hyperaldosteronism

S/S Thirst Can be accompanied by polyuria Diarrhea Sweating Neurologic disorders

TX Objectives

Correct triggering cause Correct osmolarity Normalization of ECF

Hypernatremia w/ hypovolemia Isotonic solutions until no signs of dehydration

Continue to use hypotonic solutions until correction of hypernatremia 0.45% saline solution 5% dextrose solution

Hypernatremia w/o hypovolemia Water PO If not possible, parenteral 5% dextrose

K+ Renal excretion is accelerated w/ ACTH & cortisone Increased serum concentration of K+ produces a clinical effect on

cardiac muscle Decreased ECF concentration of K+ produces weakness w/ loss of

smooth & striated muscle tone, along w/ circulatory failure Hypokalemia < 3.5 mEq/L

Severity Mild: 3-3.5 mEq/L or a deficit of 150-300 mEq Moderate: 2.5-3 mEq/L or a deficit of 300-500 mEq Severe: < 2.5 mEq/L or a deficit of > 500 mEq

Causes GI loss: diarrhea, laxatives Renal loss: hyperaldosteronism, K+-wasting diuretics,

penicillin, Amphotericin B Intracellular changes (alkalosis) Malnutrition

S/S Weakness, fatigue Paralysis, respiratory difficulty Muscle disorder (rhabdomyolysis) Constipation Paralytic ileus Leg tremors

TX Minimize extensive loss of K+ & replace K+

Administration of IV K+ is recommended when arrhythmias are present or hypokalemia is severe When indicated, max replacement of K+ IV is 10-

20 mEq/h w/ continuous ECG monitoring Hyperkalemia > 5.0 mEq/L

Repeat test Confirm test w/ ECG

Peaked T wave Short QT interval Fat QRS complex Slow conduction velocity

TX Average elevation (5-6 mEq/L): remove K+ from body

Diuretic: Furosemide 1mg/kg IV slow infusion Kayexalate: 15-30 in 50-100 mL of 20% sorbitol

solution Dialysis: peritoneal or hemodialysis

Moderate elevation (6-7 mEq/L): change ICF K+ NaHCO3 50 mEq IV Glucose-insulin IV Albuterol nebulizers 10-20 mg

Severe elevation (> 7 mEq/L) 10% CaCl2 at 5-10 mL IV over 2-5 minutes 50 mEq IV NaHCO3 for over 5 minutes Glucose-insulin IV Albuterol 20 mg Diuresis (40-80 mg IV furosemide) Kayexalate enema Dialysis

Anions in body water include Cl-, HCO3-, HPO4- Organ monitor of hydro-electrolytic disorders

Of volume Substance: water Organ: kidney Manifestation: oliguria, anuria

Of concentration Substance: sodium Organ: brain Manifestation: coma

Of composition Substance: potassium Organ: muscle Manifestation: ileus, arrhythmias, weakness

Increase in requirements Increase HR Postural changes in pulse Hypotension Decrease in diuresis Decrease in capillary filling Lab data: Na, urea, osmolarity

Hydro-electrolytic management Delay recuperation of patients Is a frequent cause of morbidity Is a cause of death MC in surgical patients

Combined depletion w/ dehydration Depletion vs dehydration

Depletion (dehydration) Affects intravascular & interstitial space (ICF &

interstitial) Loss of isotonic fluid (hypotonic) Fast velocity of development of disorder (slow) Shock hemodynamic state (normal)

Fluid therapy w/ isotonic solution (w/ hypotonic solution) Velocity of TX in minutes (infusion in hours)

Hyponatremia Hypokalemia Loss in surgical patients

Internal loss Sequestration of liquids

Severe pancreatitis Sepsis Metabolic ileus Intestinal obstruction

Blood loss Transoperative hemorrhage GI hemorrhage Hemorrhagic phase of DIC Fractures of the pelvis & long bones

External loss Evaporation via integral barriers

Hyperthermia Hyperventilation

Evaporation via loss of barriers Extensive burns Transoperative exposure of serous cavities Open abdomen for management of abdominal sepsis

GI loss V/D Drainage or GI aspiration Spontaneous fistulas Crohn’s disease Posttraumatic fistulas Surgical fistulas: external derivation of biliary tree Ileostomy, colostomy, jejunostomy, duodenostomy

Loss d/t drains Peritoneal drains Pleural drains Drains in spaces created by surgical dissection

UTI loss Osmotic polyuria (mannitol, hyperglycemia) Use of diuretics

Fluid therapy: restoration of liquids Fluid therapy in shock is based on the rescue & maintenance of renal

function, considering diuresis as a monitor of perfusion Depending on the type & rate of loss, establish the type & speed of

replacement The correction of intravascular volume depletion must be made

in minutes, while a hydro-electrolytic correction (which is not life-threatening) must be made w/in 24-48 hours

In patients w/ hypovolemia, 50% of the volume is given in the

first administration, and then given in thirds or quarters Crystalloids

Establish circulating volume (Na concentration) Short half-life (30-40 sec) Spread to interstitium (edema) Dilution of plasma proteins Contains water, electrolytes, a/o sugars Prepared

NaCl 0.9% Dextrose 5% Ringer’s lactate

Colloids Increase plasma osmotic pressure & retain water in intravascular

space Prolonged half-life Establish circulating volume Natural colloids

Plasma Albumin

Hyper-oncotic Half-life of 24 hours High cost Risk of anaphylaxis

Synthetic colloids Gelatin: half-life of 4-5 hours

Haemaccel: 330-390 mmHg Gelofusin: 465 mmHg

Dextran Dextran 40 Dextran 70

Heta-almidon Penta-almidon

Combination of crystalloids & colloids Parameters of suspending liquids

Decrease in HR below 120 BP Normal urinary flow High pressure of filling

Acute loss Pathologic: replenish volume-by-volume w/ Hartmann solution Insensitive: 0.5 ml/kg/hr + 10% for each C of temperature above 38C

Care in management w/ liquids H2O: During input of load, can auscultate frequently wheezing in the

pulmonary fields that can indicate volume overload Na: The correction of sodium is not done rapidly, but the max changes per

day in serum sodium concentration is 8 mEq/L/d for women (10 for men) K: Via peripheral vein, the max concentration of K per L of solution is 40

mEq/L, and the max velocity of input is 10 mEq/hour. No input of K+ in

the immediate postop period Dextrose: in patients w/ metabolic response in the lesion, 100 g/d of

dextrose limits 50% of catabolism of proteins (Gamble principle), which is approximately 1.5 g/kg/day. In cases of hyperglycemia, dextrose solutions can initiate when the glucose level reaches 250 mg/dL, and an insulin scheme is established

NUTRITION IN THE SURGICAL PATIENT 40-70% of hospitalized patients in any moment, have malnutrition

MC is marasmus-type malnutrition (protein-caloric malnutrition) Input of preop nutrition during 7-10 days diminishes morbidity & mortality

associated w/ surgery Surgical patients present 3 problems in basic nutrition

Secondary malnutrition to prolonged postop fast related to postop complications

Chronic malnutrition in surgical candidates that have lost weight as a consequence of their disease

High energy demands in polytraumatic & burn patients, due to the severity of their disease

Transcendence of salvation of proteins Intestinal mucosa, immune system, and renal metabolism requires high

quantities of glutamine Proteins meet a un-substitutable biologic function Its consumption to obtain energy corresponds to loss of specific

functions Malnutrition

Any state in which nutritional deficit affects health Disorder of body composition characterizes by excess of ECF & deficit of

muscle mass Causes of malnutrition in surgery

Previous & prolonged situation of fast & semi-fasting Uncompensated increase in nutritional requirements taxing the disease Malattention on the part of professionals in attending to the patient Complication of medical/surgical TX of disease Nutrients administered via an inadequate route

Consequences of malnutrition Affect musculature Affect function of respiratory muscles Facilitate the presence of cardiac abnormalities (loss of muscle mass &

decrease in CO) Harmful effects over mass & function of enterocytes & colonocytes Delay of scarring of wounds Alter immune response

Evaluation of nutritional status Capacity of protein synthesis

Visceral: pre-albumin, transferring Muscular: nitrogen balance

Immunity

Lymphocyte count Response to Ag Markers of inflammation

Organic reserve Fat: impedance Muscle: force

Visceral proteins The mass of visceral proteins can be evaluated from serum concentrations

of transport proteins synthesized in the liver Albumin is easy to determine

2.8-3.5 g/dL = mild malnutrition 2.1-2.7 g/dL = moderate malnutrition < 2.1 g/dL = severe malnutrition

Preoperative nutritional support Conserve or improve nutritional status before surgery Diminish perioperative morbidity & mortality Prevent postoperative malnutrition Prevent depletion in hypercatabolic states Contraindications

Hemodynamic instability Not recuperable patient

Parenteral nutrition Administration of nutrients via venous route w/ specific catheters to cover

the energy needs & maintain an adequate nutritional status in those patients where enteral route is inadequate, insufficient or contraindicated

TPN = when it is the only input of nutrients PPN (partial parenteral nutrition) = when other inputs of nutrients as well The complications in perfusion of parenteral nutrition are related to the

catheter, the manipulation of system, and the solution of parenteral nutrition Peripheral parenteral nutrition

In smaller veins In relatively low requirements For short time (max 2 weeks) Indications

Intestinal inflammatory diseases Malabsorption syndrome Pancreatic insufficiency Gastrectomy Radiotherapy & chemotherapy

Central parenteral nutrition Used in patients w/ greater requirements Resectable gastric cancer, in which you can recuperate nutritional

status as fast as possible In ICU

Digestive indications Neonatal, congenital, or acquired pathologies Surgical interventions Intestinal malabsorption

Severe acute pancreatitis Post-chemotherapy, post-radiation Intestinal pseudo-obstruction Irreversible vomiting Cheilous ascites Chylothorax

Extra-digestive indications Hypercatabolic state: sepsis, polytruauma, burns, neoplasias,

transplants, cachexia Pre-term newborns of low weight Visceral failure: hepatic insufficiency or acute renal insufficiency Oncology: severe mucositis

Proteins In fasting, catabolized 75g of muscle protein

Need to ingest 1-1.5g of protein per kg to maintain reserve 6.25 g of protein contains 1 g of nitrogen

CHO Constitutes 50% of caloric input in diet Each g of monohydrate dextrose inputs 3.4 calories W/ administration of 100-150 g of glucose in fasting, which is 50% of

protein Lipids

Require 25g to favor absorption of lipid soluble vitamins In fast, break down 160g of fat in 24 hours Oxidation of 1g of lipids yields 9 Kcal

Oligoelements: Zn, Cu, Cr, Se Deficit of zinc doesn’t help wound scarring Cr potentiates action of insulin Se is an antioxidant Mn is a procoagulant

Iron Men: 1000mg (women: 300-500mg) Parenteral dosage is 0.5-1.0 mg/day

Vitamin C Cofactor in collagen synthesis Participates in tissue reparation

Standard formulas Dextrose = 10-25% of central parenteral nutrition (5% of peripheral) AA = 4.25% of central parenteral nutrition (same) Na+ = 36.5 mEq/L or a K+ = 36.5 mEq/L

Advantages of parenteral nutrition 100% absorption Continuous infusion Very complete Does not use digestive use, which is still useful in a specific group of

patients Disadvantages of parenteral nutrition

Alter the quality of mucosa & intestinal transit, producing bacterial

translocation & problems of eating later More expensive: require major manipulation, monitorization & special

physical place Complications are grave, w/ infection of the central venous catheter, w/

sepsis for nosocomial microorganisms Require change in all of central venous system

Increment of caloric dose Elective surgey = 10% of stress factor Trauma = 10-30% of stress factor Sepsis = 50-80% of stress factor

Enteral nutrition Technique to support nutrition which consists of administration of nutrients

Directly into GI tract, find tube in liquid environment Indications

GI tract is functional but… Not able to use optimally nutrients PO

d/t severe D, short intestinal syndrome If the needs are extremely increased and the patient cannot cover

them w/ ingestion burn patients, malnutrition

When the patient cannot swallow Advantages

Most physiologically normal means of input More trophic stimulation of GI tract Cheaper Easier to care for Require less invasive procedures for the patient

Contraindications Intestinal obstruction Intolerance to formula Diarrhea Gluten enteropathy Hypoperfusion

Routes of choice NG tube Trans-pyloric tube: nasoduodenal or nasojejunal Gastrostomy

Percutaneous endoscopy Radiology Surgery

Jejunostomy Types of solution

Polymeric Ensure/ Ensure fiber Osmolite 1 cal/cc (low osmolarity) Pulmocare (low in CHO high in proteins) Glucal Bott (low in CHO) Nephro, Suplena (nephropathy)

Advera (1 cal/cc) Alitreg (metabolic distress) Sevite 1 cal/cc (low osmolarity, to correct D or constipation)

Peptidic: when proteins are hydrolyzed Elemental: when proteins are in the form of AA

Complications Bronchoaspiration Infectious Metabolic (inadequate nutrients) Mechanic (obstruction of NG tube)

For specific pathologies Hepatic: decrease dosage of lipids or suppress input Pneumo: decrease CHO & increase lipids Renal: decrease input of proteins, Na, K, P, Mg Sepsis: increase immuno-nutrients, input AA for catabolism

Immuno-nutrition Arginine

High demand in catabolic states and in growth Improves the response of T cells to mitogens Improves the response to late sensitivity

Glutamine Energetic substrate of enterocyte Its precursor, glutamate, represents 61% of AA in plasma Favors support of enteral mass & mucosal integrity

Nucleotides Forms part of nucleic acids Are necessary for production of T cells, epithelial cells, &

interleukins Omega-3 FA

Does not produce Immunosuppression of Burns: increase proteins and non-protein calories