acute lung injury and ARDS

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PULMONARY
COMPLICATIONS
PULMONARY COMPLICATIONS
• Occur in up to 15% of general anaesthetic and
major surgery and include:
– Atelectasis
– Pneumonia
– Pulmonary Edema, Acute Lung Injury, and Adult
Respiratory Distress Syndrome
– Pulmonary Embolism and Venous
Thromboembolism
Atelectasis (alveolar collapse):
Caused
– airways obstructed, usually by bronchial secretions.
– anesthetic, abdominal incision, and postoperative narcotics,
Risk
― heavy smokers, obese, and have pulmonary secretions
Symptoms
– slow recovery from operations, poor colour, mild tachypnea, tachycardia
and low-grade fever
– the alveoli in the periphery collapse and a pulmonary shunt may occur
Prevention is by pre-and post-operative physiotherapy
– pain control, take deep breaths
In severe cases
– positive pressure ventilation may be required
Pneumonia
requires antibiotics, physiotherapy.
Aspiration pneumonitis:
• Sterile inflammation of the lungs from inhaling gastric
contents
Symptoms
• vomiting or regurgitation with rapid onset of
breathlessness and wheezing.
• Non-starved patient undergoing emergency surgery is
particularly at risk
• May help avoid this by use of oral antacids or
metoclopramide
• Mortality is nearly 50%
Pneumonia
requires urgent treatment
• bronchial suction, positive pressure ventilation,
prophylactic antibiotics and IV steroids
Prevention of aspiration
• a period of no oral intake
• usually 6 hours after a night meal
• 4 hours after clear liquids
• a longer period for diabetics
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
Etiology
• A wide variety of injuries to the lungs or
cardiovascular system, or both.
• Three of the most common manifestations
– pulmonary edema, acute lung injury, and ARDS
Conditions Leading
• Increased Hydrostatic Pressure
• Altered Permeability State
• Mixed or Incompletely Understood Pathogenesis
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
Conditions Leading
Increased Hydrostatic Pressure
 Acute left ventricular failure
 Chronic congestive heart failure
 Obstruction of the left ventricular outflow tract
 Thoracic lymphatic insufficiency
 Volume overload
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
Conditions Leading (continued)
Altered Permeability State
 Acute radiation pneumonitis
 Aspiration of gastric contents
 Drug overdose
 Near-drowning
 Pancreatitis
 Pneumonia
 Pulmonary embolus
 Shock states
 Systemic inflammatory response syndrome and multiple organ failure
 Sepsis
 Transfusion
 Trauma and burns
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
Conditions Leading (continued)
Mixed or Incompletely Understood Pathogenesis
 Hanging injuries
 High-altitude pulmonary edema
 Narcotic overdose
 Neurogenic pulmonary edema
 Postextubation obstructive pulmonary edema
 Re-expansion pulmonary edema
 Tocolytic therapy
 Uremia
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
pulmonary edema
 often have a corresponding cardiac history or a
recent history of massive fluid administration (or
both).
 abnormal chest radiograph
Management
 Requires intensive care with mechanical ventilation
with positive-end pressure
 oxygen via facemask in mild cases
 intubation in more severe cases
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
acute lung injury and ARDS
 tachypnea, dyspnea, and increased work of breathing, as
manifested by exaggerated use of the muscles of
breathing.
 Cyanosis is associated with advanced hypoxia and is an
emergency
 In patients with impending respiratory failure
 tachypnea, dyspnea, and air hunger
 Auscultation of the lung
 very poor breath sounds associated with crackles .
 Arterial blood gas
 presence of a low Pao2 and a high Paco2
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
acute lung injury and ARDS
Management
 initiated by immediate intubation plus careful
administration of fluids and invasive monitoring with
a Swan-Ganz catheter to assess wedge pressure and
right-sided heart pressure.
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
acute lung injury and ARDS
Management
 maintaining the patient on the ventilator with
assisted breathing while healing of the injured lung
takes place
 severe acute lung injury or ARDS is initially placed on
an Fio2 of 100% and then weaned to 60% as healing
takes place.
Pulmonary Edema, Acute Lung Injury, and
Adult Respiratory Distress Syndrome
acute lung injury and ARDS
Pulmonary Embolism and Venous
Thromboembolism
• serious postoperative complication
• DVT is very commonly related to grade of surgery.
• Many cases are silent
– present as swelling of leg, tenderness of calf muscle and
increased warmth
• Diagnosis
– venography or Doppler ultrasound.
Pulmonary Embolism and Venous
Thromboembolism
Risk Factors for Venous Thromboembolism
CATEGORY
FACTORS
General factors
Advancing age
Hospitalization or nursing home
(with or without surgery)
Neurologic disease (plegia and paresis)
Cardiomyopathy, myocardial infarction, or heart
failure secondary to valve disease
Acute pulmonary disease (adult respiratory distress
syndrome and pneumonia)
Chronic obstructive lung disease
Varicose veins
Pulmonary Embolism and Venous
Thromboembolism
Risk Factors for Venous Thromboembolism
CATEGORY
FACTORS
Inherited thrombophilia
Protein C,S deficiency
Antithrombin III deficiency
Dysfibrinogenemia
Factor V Leiden mutation
Prothrombin gene mutation
Anticardiolipin antibody
Paroxysmal nocturnal hemoglobinemia
Pulmonary Embolism and Venous
Thromboembolism
Risk Factors for Venous Thromboembolism
CATEGORY
FACTORS
Acquired thrombophilia
Malignancy
Inflammatory bowel disease
Heparin-induced thrombocytopenia
Trauma
Major surgery
Nephrotic syndrome
Systemic lupus erythematosus
Pregnancy/postpartum
History of venous thromboembolism
Pulmonary Embolism and Venous
Thromboembolism
Pulmonary embolism
Pulmonary Embolism and Venous
Thromboembolism
Pulmonary embolism
• Diagnosis
– ventilation/perfusion scanning and/or pulmonary
angiography or dynamic CT
• Management
– intravenous heparin or subcutaneous low
molecular weight heparin (LMWH),oral warfarin.
– goal of reaching an INR of 2.5.
ENDOCRINE
COMPLICATIONS
ENDOCRINE
COMPLICATIONS
•
•
•
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Adrenal Insufficiency
Hyperthyroid Crisis
Hypothyroidism
Syndrome of Inappropriate Antidiuretic
Hormone Secretion
Adrenal Insufficiency
Chronic adrenal insufficiency
Etiology
• Adrenal insufficiency is an uncommon but potentially lethal
condition associated with failure of the adrenal glands to produce
adequate glucocorticoids
1. Primary adrenal insufficiency
– most frequently due to autoimmune adrenalitis (Addison's disease), in
which the adrenal cortex is destroyed by cytotoxic lymphocytes.
2. Secondary adrenal insufficiency
– most commonly caused by long-term administration of pharmacologic
doses of glucocorticoids.
– Chronic use of glucocorticoids causes suppression of the
hypothalamic-pituitary-adrenal axis (HPA), induces adrenal atrophy,
and results in isolated adrenal insufficienc
Adrenal Insufficiency
Acute adrenal insufficiency
Etiology
• a result of abrupt cessation of pharmacologic
doses of chronic glucocorticoid therapy,
• surgical excision or destruction of the adrenal
gland (adrenal hemorrhage, necrosis, or
thrombosis in patients with sepsis or
antiphospholipid syndrome),
• surgical excision or destruction (postpartum
necrosis) of the pituitary gland.
Adrenal Insufficiency
 Symptoms and signs
 fatigue, weakness, anorexia, weight loss, orthostatic
dizziness, abdominal pain, diarrhea, depression,
hyponatremia, hypoglycemia, eosinophilia, decreased
libido and potency.
 Patients with primary hypoadrenalism
 elevated plasma levels of corticotropin
(hyperpigmentation of the skin and mucous membrane).
 Patients with secondary disease in contrast,
 initially have neurologic or ophthalmologic symptoms
(headaches, visual disturbances) before showing signs of
HPA axis disease (hypopituitarism).
Adrenal Insufficiency
Adrenal Insufficiency
Treatment
 detailed instruction of patients receiving chronic
corticosteroid therapy
 Adequate perioperative corticosteroid administration.
 In the critically ill
 a high index of suspicion can prevent a fatal outcome. A stress dose of
hydrocortisone (100 mg) may be given with induction of anesthesia.
 For minor surgical procedures,
 usual maintenance dose is continued postoperatively.
 For major surgical procedures,
 a stress dose (100 mg) is continued every 8 hours until stable or free of
complications and then tapered to the usual maintenance dose.
Adrenal Insufficiency
Hyperthyroid Crisis
Etiology
• Thyroid crisis is a medical emergency that occurs in
thyrotoxic patients with toxic adenoma or toxic
multinodular goiter
• most often in patients with Grave's disease.
• The crisis is frequently precipitated by a stressful
event and characterized by exacerbation of
hyperthyroidism and decompensation of one or
more organ systems.
• Mortality is high, ranging from 20% to 50% if the
crisis is unrecognized and left untreated.
Hyperthyroid Crisis
Clinical manifestations of hyperthyroidism
– nervousness, fatigue, palpitations, heat intolerance,
weight loss, atrial fibrillation (in the elderly),
– ophthalmopathy characterized
• eyelid retraction or lag, periorbital edema, and proptosis.
– The onset of thyroid crisis is sudden and characterized by
accentuation of the symptoms and signs of thyrotoxicosis
and organ system dysfunction
• hyperpyrexia, tachycardia, dehydration , central nervous system
dysfunction (delirium, psychosis, seizure, coma), cardiac
manifestations, GI symptoms, and liver dysfunction.
Hyperthyroid Crisis
diagnosis of thyrotoxicosis
• elevated levels of circulating thyroid hormone and suppressed
thyroid-stimulating hormone (TSH) levels
Hyperthyroid Crisis
• elevated levels of circulating thyroid hormone and suppressed
thyroid-stimulating hormone (TSH) levels
• Treatment
hypothyroidism
Etiology
• Hypothyroidism is characterized by low systemic
levels of thyroid hormone and may be exacerbated in
the postoperative period in patients with preexisting
chronic hypothyroidism or as a result of severe
stress.
• Severe illness, physiologic stress, and drugs may
inhibit peripheral conversion of T4 to T3 and induce a
hypothyroid-like state.
• Hypothyroidism may be primary (surgical removal,
ablation, or disease of the thyroid gland), secondary
(hypopituitarism), or tertiary (hypothalamic disease).
hypothyroidism
Presentation and Diagnosis
• Patients with chronic hypothyroidism may be asymptomatic
or rarely have the severe form (myxedema coma)
characterized
– coma, loss of deep tendon reflexes, cardiopulmonary collapse
– high (∼40%-50%) mortality.
• The majority, demonstrate
– cold intolerance, constipation, brittle hair, dry skin, sluggishness,
weight gain, and fatigue.
• The impact of hypothyroidism  cardiovascular system
– bradycardia, hypotension, impaired cardiac function, conduction
abnormalities, pericardial effusion, and increased risk for CAD.
• In the critically ill (trauma, sepsis)pulmonary function
– a predisposition to pleural effusion, and susceptibility to
hypothermia.
hypothyroidism
Presentation and Diagnosis
• The ECG usually shows bradycardia, low voltage,
and prolonged PR, QRS, and QT intervals.
primary hypothyroidism
– serum total T4, free T4, and free T3 levels are low,
whereas TSH is elevated.
secondary hypothyroidism
• TSH, the free T4 index, and free T3 are low.
hypothyroidism
Treatment
• Patients with known hypothyroidism who are receiving
replacement hormonal therapy and are in the euthyroid
state
– do not require any special treatment before surgery but are
instructed to continue taking their medications.
• In patients with symptomatic chronic hypothyroidism
– surgery is postponed until a euthyroid state is achieved.
• Patients with myxedema coma or those showing clinical
signs of significant hypothyroidism (severe postoperative
hypothermia, hypotension, hypoventilation, psychosis, and
obtundation)
– immediately treated with thyroid hormone, concomitant with
the IV administration of hydrocortisone, to avoid an addisonian
crisis. IV levothyroxine or triiodothyronine may be given until
oral intake is possible.
Syndrome of Inappropriate
Antidiuretic Hormone Secretion
Etiology
– The syndrome of inappropriate antidiuretic
hormone secretion (SIADH) is the most common
cause of chronic normovolemic hyponatremia.
– Hyponatremia is defined as a serum sodium
concentration of less than 135 mmol/L
– hyponatremia despite all attempts to correct the
imbalance in the presence antidiuretic activity
from elevated arginine vasopressin
Syndrome of Inappropriate
Antidiuretic Hormone Secretion
Etiology
– Disorders and conditions that predispose to this
relatively rare condition
• trauma, stroke, antidiuretic hormone–producing
tumors, drugs (ACE inhibitors, dopamine, NSAIDs), and
pulmonary conditions.
Syndrome of Inappropriate
Antidiuretic Hormone Secretion
Clinical characteristics
• anorexia, nausea, vomiting, obtundation, and
lethargy. With more rapid onset, seizures, coma,
and death can result.
The cardinal criteria of SIADH include
– hyponatremia
– hypotonicity of plasma,
– urine osmolality in excess of plasma osmolality,
increased renal sodium excretion
– absence of edema or volume depletion
– normal renal function.
Syndrome of Inappropriate
Antidiuretic Hormone Secretion
Treatment
• Management of SIADH includes treatment of the underlying
disease process and removal of excess water (i.e., treatment of the
hyponatremia).
• Fluid restriction is the mainstay of management of chronic SIADH.
• IV administration of normal saline is used only in significantly.
• Diuretics such as furosemide occasionally help correct the
imbalance.
• In some cases, IV administration of 3% saline solution may be
required, but correction must be done in a constant, sustained
fashion because overly rapid correction can result in seizure activity.
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