The presentation deals with the basics of pre anesthetic checkups, its only for the educations purpose!
Any kind of replication, modifications and republication is strictly prohibited.
All Rights reserved to the Author. 2016
The presentation deals with the basics of pre anesthetic checkups, its only for the educations purpose!
Any kind of replication, modifications and republication is strictly prohibited.
All Rights reserved to the Author. 2016
Chronic Obstructive Pulmonary Disease BY
Dr Akram Yousuf
Resident Internal Medicine
Liaquat University of Medical Health and Sciences Jamshoro Pakistan
How to ventilate COPD and ARDS in Intensive care unit. safe lung ventilation. PEEP, Tidal volume, mode of ventilation. limits of ventilation. ventilator alarms
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
2. TREYresearch
RespiratoryDiseases
• Postoperative respiratory complications are more common in those who smoke.
• The risk declines by 50% after only 8 weeks of smoking cessation, although patients
who stop smoking for less than 8 weeks before surgery have a higher risk for
complications than those who continue to smoke.
• Cigarette smoke also results in elevated levels of carboxyhemoglobin (CoHb), which
predisposes the patient to perioperative hypoxia.
• Pulse oximetry cannot detect CoHb.
• An arterial blood gas (ABG) is required to measure the CoHb.
• CoHb and nicotine both increase the potential for cardiac complications including
ventricular fibrillation.
• This additional risk can be eliminated with smoking cessation for 24 hours.
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RespiratoryDiseases
• The most common screening tool continues to be the chest x-ray
• The yield is relatively low unless diffuse parenchymal disease, pulmonary edema,
pneumonia, or advanced chronic obstructive pulmonary disease (COPD) is present.
• Pulmonary peak flow can be easily measured with an office peak flowmeter.
• Pulmonary function testing (PFT) is the gold standard in evaluating pulmonary
function; it measures lung volumes and lung dynamics including flow rates
throughout the respiratory cycle.
• The forced expiratory volume in 1 second (FEV1) and its relationship to the forced vital
capacity (FVC) are particularly useful to quantitate disease severity and stratify
patients.
• The measurement of the partial pressures of oxygen and carbon dioxide, pH, and
base excess allows the net effect of pulmonary disease on oxygenation to be seen.
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RespiratoryDiseases
• The net result of most respiratory diseases is hypoxemia that may develop from one
of four mechanisms:
1. Hypoventilation; a decrease in respiratory rate or vital capacity; asthma, chronic
COPD, obstructive sleep apnea, pneumonia, chest trauma, narcotics, neurologic
disease, and idiopathic pulmonary fibrosis.
2. Diffusion impairment; may be due to idiopathic pulmonary fibrosis or acute
respiratory distress syndrome.
3. Ventilation-perfusion mismatching; many processes including Pulmonary Edema
4. Shunting; PE, Pneumonia, Atelectasis, Cardiac Septal Defects and Chronic Liver
Disease.
• Management of patient with Hypoxemia and Increased work of breathing requires
intervention.
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RespiratoryDiseases
• The cause for the hypoxemia must be known.
• Treatment involves the administration of oxygen using one of several methods, all of
which increase the fractional concentration of inspired oxygen (FiO2).
• The effect of varying the method of oxygen delivery on the FiO2 should not be
underestimated.
• Nasal cannula (1 L/min increases the FiO2 by 4% to a maximum of 40% at 6 L/min).
• Rebreathing facemask (increases the FiO2 to 60% at 10 L/ min).
• Non-rebreathing facemask (increases the FiO2 to 90% at 10 L/min).
• CPAP/BiPAP (continuous positive airway pressure/bi-level positive airway pressure)
with positive pressure (increases the FiO2 to 80%).
• Intubate/tracheostomy (increases the FiO2 to 100%)
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Asthma
• Bronchial hyper-responsiveness and reversible bronchoconstriction due to smooth
muscle contraction leading to reduced minute ventilation and hypoxemia.
• Signs and symptoms; episodic dyspnea, shortness of breath, limitation in activity,
expiratory wheezing, cough, chest tightness and pain
• Status Asthmaticus.
• Exacerbation depends on:
• The occurrence of pain and stress
• Aspiration during induction
• Presence of an unrecognized preoperative upper respiratory tract infection.
• History of emergency room visits and the need for intubation should be reasons for
concern.
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Asthma
• Patients with significant asthma as evident by these indicators are probably ASA class
III patients and are probably not good candidates for office-based sedation or
general anesthesia.
• Bronchospasm that heralds an asthma attack can occur rapidly and be difficult to
manage even with positive-pressure ventilation and intubation.
• This is in part due to the combined effect of smooth muscle contraction, edema, and
mucous plugging.
• Diagnosis of asthma:
• Appropriate history of asthma-like symptoms
• PFT that indicates a reduction in FEV1, normal vital capacity, reduced FEV1/FVC
(proportional to severity)
• Increase in FEV1 by 10% with bronchodilator treatment.
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Asthma
• Peak expiratory flow rate is best used to monitor asthma over time and identify
potential exacerbations.
• A decline in the peak flow rate to less than 80% of baseline would suggest
exacerbation and elective surgery should be postponed.
• Classification; Intermittent, Mild Persistent, Moderate Persistent or Severe Persistent
• Frequency and severity of symptoms, FEV1, and peak flow are all used to categorize
patients into one of these groups.
• The treatment of exacerbations often requires that a SABA be administered by
metered-dose inhaler (MDI) or nebulizer every 2 hours as needed.
• Continuous nebulized treatment may be beneficial in children.
• Anticholinergic medication can also be administered by MDI or nebulizer every 6
hours as needed.
• A short course of oral or parenteral corticosteroid over a week may also be needed
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Asthma
• Medications for Asthma
• Short-acting beta agonist (SABA) such as albuterol.
• Inhaled corticosteroids such as fluticasone.
• Anticholinergic medications such as ipratropium or tiotropium.
• Long-acting beta agonists (LABAs) such as salmeterol or formoterol.
• Leukotriene receptor antagonists such as montelukast and zafirlukast.
• Cromolyn.
• Theophylline.
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ChronicObstructivePulmonaryDisease
• Emphysema and chronic bronchitis are the two major respiratory diseases within
COPD.
• Emphysema is characterized by dilated and collapsed airways with alveolar
destruction secondary to alpha 1 antitrypsin deficiency as a result of smoking or
congenital deficiency.
• Chronic bronchitis is characterized by increased airway secretions and mucous
production, often secondary to smoking.
• A patient with emphysema is often described as a “pink puffer”.
• A patient with chronic bronchitis is often described as a “blue bloater.”
• The net result of both diseases is retention of carbon dioxide and eventually
hypoxemia.
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COPD
• Symptoms include; Chronic cough, Sputum production, Shortness of breath,
Decreased functional Status, Wheezing and Barrel-shaped chest.
• As disease advances, patients may begin to expire with pursed lips, which increases
intrathoracic pressure to help stent their airways open.
• The Diagnosis; appropriate history supplemented with additional tests
• PFTs reveal a reduction in FEV1, no change in vital capacity, and a reduction in the
FEV1/FVC.
• ABGs are particularly helpful and reveal an increase in the partial pressure of carbon
dioxide, a decrease in the partial pressure of oxygen, and respiratory alkalosis.
• The chest x-ray reveals a loss of lung markings, hyperinflation, and a flattened
diaphragm.
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ChronicObstructivePulmonaryDisorder
• If patients continue to smoke, complications will be higher.
• Smoking cessation should occur longer than 8 weeks before the planned surgical
procedure.
• Elective surgery in the face of a COPD exacerbation is contraindicated.
• COPD can be classified as mild, moderate, severe, and very severe.
• Well hydrated and use humidified oxygen when needed to reduce the inspissation of
secretions.
• Patients with mucopurulent sputum are best treated with a course of antibiotics such
as azithromycin, trimethoprim/ sulfamethoxazole, or amoxicillin.
• Complications can be Perioperative or Postoperative.
• The perioperative concerns are typically anesthesia related.
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ChronicObstructivePulmonaryDisorder
• Nitrous oxide is best avoided due to its blood/gas coefficient and the potential to
accumulate within the multiple bullae associated with COPD, which can rupture.
• Ventilator plateau pressures should be kept to a moderate level to further reduce this
risk.
• Peak flow pressures will typically be increased to allow for a short inspiratory and
prolonged expiratory time [crucial to reduce the likelihood of auto-PEEP (auto
positive-end-expiratory pressure)].
• Oxygen delivery with nasal cannula or facemask.
• SABA such as an albuterol MDI or nebulizer as needed.
• Anticholinergic medication such as an ipratropium MDI or nebulizer as needed.
• Corticosteroid burst given orally or intravenously over 5 days (prednisolone 1
mg/kg/day).
• The need to intubate patients who are doing poorly should be considered early.
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ChronicObstructivePulmonaryDisorder
• The potential concern of administering oxygen to COPD patients who rely on a
hypoxic respiratory drive is more theoretical than real.
• Any patient with COPD who is hypoxemic as a result of the disease should be
treated aggressively with oxygen.
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Pneumonia
• Nosocomial pneumonia may occur in the postoperative period.
• It may be associated with the use of mechanical ventilation, at which time it is
referred to as “ventilator-associated pneumonia.”
• The development of pneumonia may be influenced by:
• The use of perioperative antibiotics.
• The placement of nasogastric feeding tubes
• The propensity for aspiration.
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Pneumonia
• The most common causative organisms associated with nosocomial pneumonia are:
• Streptococcus pneumoniae
• Staphylococcus aureus
• Pseudomonas aeruginosa
• Acinetobacter species
• Anaerobic organisms.
• The net result is hypoxemia and sepsis.
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Pneumonia
• Signs and Symptoms:
• Dyspnea
• Shortness of breath
• Fever
• Chest pain
• Decreased breath sounds
• Fremitus
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Pneumonia
• Additional findings are a chest x-ray or computed tomography (CT) scan indicating:
• Infiltration or consolidation of lung parenchyma
• Para-pneumonic pleural effusion
• Broncho-alveolar lavage with cultured organisms
• Positive blood culture
• Increased white blood cell count.
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Pneumonia
• The diagnosis should be considered in any patient on a ventilator who develops fever
and the need for increased ventilatory support including inspired oxygen pressure
and PEEP.
• The peak pressures are often also elevated secondary to reduced lung compliance.
• The treatment of pneumonia includes the use of parenteral antibiotics, which may
involve either monotherapy or combination therapy.
• The need to convert patients from an endotracheal tube to a tracheotomy and the
timing of this continue to be controversial
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PulmonaryEmbolus
• More than 95% of PEs are from the deep veins of the legs.
• These travel to the lungs, leading to respiratory and cardiovascular compromise.
• Most emboli are clinically silent owing to their small size.
• Risk factors include:
• Smoking
• Contraceptives,
• Pregnancy
• Advance age
• Malignancy
• Abdominal and orthopedic surgery
• Hereditary coagulation disorders such as Anti-thrombin III deficiency, Factor V
Leiden, and protein C and S deficiency
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PulmonaryEmbolus
• Prevention with sequential calf compressors, thromboembolic deterrent stockings,
and perioperative UFH or LMWH is important.
• All patients who undergo surgery should be considered at risk for PE.
• General anesthesia and surgery produce a pro-thrombotic state that is compounded
by bed rest.
• Early ambulation and appropriate preventive measures afford the best opportunity to
reduce the risk of PE.
• Signs and symptoms include chest pain, shortness of breath, dyspnea, sinus
tachycardia, hemoptysis, a swollen and painful leg, and pain on dorsiflexion of the
foot (Homan’s sign).
• An initial ABG with a large alveolar-arterial (A-a) gradient would be suspicious for PE.
• A CT scan of the chest with contrast (PE protocol) can identify sub-segmental
pulmonary arteries and emboli within them.
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PulmonaryEmbolus
• A duplex ultrasound of the leg veins should also be obtained.
• The sensitivity of this scan is highest for deep venous thrombosis (DVT) between the
knee and the groin.
• The D-dimer assay is a relatively simple blood test that measures the level of fibrin
degradation products.
• A positive D-dimer may be due to a multitude of conditions
• Negative D-dimer virtually excludes DVT/PE, reflecting the high negative predictive
value.
• An ECG most often reveals a nonspecific sinus tachycardia, although the classic
pattern of an S wave in lead I and a Q wave and inverted T wave in lead III may be
seen, reflecting right ventricular strain.
• Pulmonary angiography remains the gold standard but is infrequently used because it
is invasive.
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PulmonaryEmbolus
• The treatment of PE may include:
• Initial heparin bolus followed by
• Heparin drip.
• Alternatively, enoxaparin or fondaparinaux can be administered subcutaneously.
• Long-term anticoagulation should also be simultaneously initiated with warfarin with
a goal INR of 2.5 to 3.
• Massive PE leading to right ventricular strain may require chemical thrombolysis or
surgical thrombectomy.
• Patients unable to be anticoagulated and patients with recurrent PE despite
anticoagulation are candidates for inferior vena cava filters to prevent the
development of PEs.
• The filters may be permanent or temporary and are themselves at risk for obstruction.
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Atelectasis
• Common postoperative outcome characterized by the segmental collapse of lung
alveoli.
• It leads to a progressive decline in lung compliance, impaired segmental ventilation,
retained secretions, and a decrease in functional residual capacity.
• The signs and symptoms include decreased breath sounds, inspiratory crackles at the
• bases, increased work of breathing, and a low-grade fever.
• The diagnosis is based on the clinical picture and temporal relationship to the
immediate postoperative period supported when indicated by chest x-ray.
• Treatment includes incentive spirometry and early ambulation.
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PulmonaryEdema
• Cardiac and non-cardiac causes.
• In normal cardiac function, it may be the result of fluid overload or it can follow
extubation as a result of upper airway obstruction leading to negative pressure
pulmonary edema (NPPE) [more common in young males].
• The net result is significant alveolar transudation and hypoxemia.
• Risk factors include:
• Obesity,
• Obstructive sleep apnea
• Maxillofacial surgical procedures.
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PulmonaryEdema
• Signs and symptoms include:
• Increased work of breathing
• Dyspnea
• Shortness of breath
• Decreased breath sounds
• Bilateral crackles.
• The diagnosis is based on the:
• Clinical suspicion
• The development in the immediate postoperative period
• Chest x-ray with diffuse infiltrates.
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PulmonaryEdema
• Treatment usually requires:
• Supplemental oxygen
• Support of the airway
• Possible re-intubation and a short period of mechanical ventilation with PEEP.
• Diuretics may be used to facilitate fluid removal but are typically not required.
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Airway
• A preoperative assessment of the airway is mandatory.
• Complications related to establishing an airway and maintaining ventilation continue
to be a source of significant patient morbidity and mortality.
• The oral and maxillofacial surgeon must:
• Carefully assess the potential for airway difficulty
• Must be in a position to appropriately prevent it when possible
• Manage it when it develops during sedation or general anesthesia.
• Prior History of sedation or GA
• Obese individuals present potentially difficult airways and, due to their weight, have a
reduced functional residual capacity, making early oxygen desaturation likely.
• Pregnancy
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Airway
• A decrease in cervical range of motion
• A decrease in the maximum incisal opening
• The presence of a retrognathic mandible all portend to a potentially difficult airway.
• Congenital conditions such as Pierre Robin, Treacher Collins, Goldenhar, Klippel-Feil,
and Down syndromes;
• Oropharyngeal infections
• Oropharyngeal tumors
• Radiotherapy patients
• Patients with TMJ ankylosis.
• The Mallampati scheme
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Airway
• the ability to support the airway can be accomplished using
• Jaw lift
• Oral or nasal airway
• Positive-pressure bag-valve-mask ventilation is mandatory.
• Laryngeal mask
• Endotracheal tube
• Cricothyroidotomy.
• Patients who present with potentially difficult airways might be better candidates for
hospital-based procedures.
• Ultimately, it is the responsibility of the surgeon and anesthesiologist to provide a
secure airway and one or more back-up plans should the unexpected difficult airway
be encountered.
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