SNAKE BITES

Snake Bites

At presentation of casualty A,B,C  of resuscitation ,some of the venomous snakes can complicate with hemorrhagic shock,cardiotoxicity

Secondary survey

1-History of the snake bites and if possible establishes whether it was venomous or not.

2-Examination of the wound inflicted can give indication whether the snake was venomous or not. Nonvenomous snakes do not produce fang marks, but rather rows of tiny puncture wounds or scratches.

3-Removal of any tight clothing on the limb or tourniquet that had been applied.

4- Obtain IV access in the non-affected limb and keep on IV fluids

5-Take vital signs continuously monitor

6-Clean the bitten part and irrigate with copious amounts of water.

7-Elevate the limb as much as possible.

8-Provide analgesia

9-Administer tetanus toxoids

10-Give prophylactic antibiotics

11-Measure circumference of the bitten part at several levels, comparing these with similar measurements carried out once on the unaffected side.

-Monitor for any continued swelling.

12-If anti venom available this can be given in the IV fluid infusion and run slowly looking out for any allergic reactions.

13-If there is continued swelling of the limb even with elevation, then fasciotomy may be necessary to prevent occurrence of compartment syndrome.

Initial investigations

1.Full blood count-Hb ,can draw blood for GXM

2.LFT-Liver transaminases ,serum bilirubin

3.Urea,electrolyte and creatinine

Urinalysis-protenuria and hematuria

4.Creatine kinase

5.Coagulation profile-  platelet count, clotting time, prothrombin time, partial thromboplastin time, fibrinogen level

6. ECG studies.

Manage any complications as appropriate:

Abnormal coagulation profile-Fresh frozen plasma transfusion.

Hemolytic anemia-Whole blood transfusion

Shock-IV fluid –crystalloids and Colloids

STATUS ASTHMATICUS

STATUS ASTHMATICUS Introduction -Status asthmaticus is an acute exacerbation of asthma that remains unresponsive to initial treatment with bronchodilators. -Patients report chest tightness, rapidly progressive shortness of breath, dry cough, and wheezing. -Typically, patients present a few days after the onset of a viral respiratory illness, following exposure to a potent allergen or irritant, or after exercise in a cold environment. Pathophysiology -Allergic inflammation in asthma begins with the development of a predominantly helper T2 lymphocyte–driven, as opposed to helper T1 lymphocyte–driven, immune milieu, perhaps caused by certain types of immune stimulation early in life. -This is followed by allergen exposure in a genetically susceptible individual. Specific allergen exposure (eg, dust mites) under the influence of helper T2 lymphocytes leads to B-lymphocyte elaboration of immunoglobulin E (IgE) antibodies specific to that allergen. -The IgE antibody attaches to surface receptors on airway mucosal mast cells. -Subsequent specific allergen exposure leads to cross-bridging of IgE molecules and activation of mast cells, with elaboration and release of a vast array of mediators. -These mediators include histamine; leukotrienes C4, D4, and E4; and a host of cytokines. -These mediators cause: ü Bronchial smooth muscle constriction ü Vascular leakage ü Inflammatory cell recruitment (with further mediator release) ü Mucous gland secretion -These processes lead to airway obstruction by constriction of the smooth muscles, edema of the airways, influx of inflammatory cells, and formation of intraluminal mucus. -In addition, ongoing airway inflammation is thought to cause the airway hyperreactivity characteristic of asthma. -Physiologically, asthma has 2 components: an early acute bronchospastic aspect marked by smooth muscle bronchoconstriction and a later inflammatory component resulting in airway swelling and edema. Early bronchospastic response Mediators, including histamine, prostaglandin D2, and leukotriene C4. These substances cause airway smooth muscle contraction, increased capillary permeability, mucus secretion, and activation of neuronal reflexes. Early asthmatic response is characterized by bronchoconstriction that is generally responsive to bronchodilators, such as beta2-agonist agents Clinical presentation History -The symptoms of asthma consist of a triad of § Dyspnea § Cough § wheezing § Chest tightness -Wheezing regarded as the sine qua non for asthma. -Cough is non productive initially then thick sputum later - Personal or family history of allergic diseases such as eczema, rhinitis, or urticaria is valuable contributory evidence. -Worsening of symptoms after exposure to recognized triggers such as pollens, dust, feathered or furry animals, exercise, viral infections, chemicals, and environmental tobacco smoke -Worsening of symptoms after taking aspirin/non-steroidal anti-inflammatory medication or use of β-blockers. -An extremely common feature of asthma is nocturnal awakening with dyspnea and/or wheezing The hallmark of asthma is that these symptoms tend to be: 􀂄 Variable 􀂄 Intermittent 􀂄 Worse at night 􀂄 Provoked by triggers including exercise Physical -Respiratory distress -Patients present with tachypnea, tachycardia, and mild systolic hypertension. -Severe asthma may give paradoxical pulse. paradoxical pulse depends on the generation of large negative intrathoracic pressures -The lungs rapidly become overinflated, and the anteroposterior diameter of the thorax increases. –barrel chest. -If the attack is severe or prolonged, there may be a loss of adventitial breath sounds, and wheezing becomes very high pitched. -The end of an episode is marked by a cough that produces thick, stringy mucus, which often takes the form of casts of the distal airways (Curschmann's spirals) and, when examined microscopically, often shows eosinophils and Charcot-Leyden crystals. - Very severe attack may cause air trapping with the chest and cause silent chest. These findings imply extensive mucus plugging and impending suffocation. Ventilatory assistance by mechanical means may be required. -Atelectasis due to inspissated secretions occasionally occurs with asthmatic attacks. - Spontaneous pneumothorax or pneumo-mediastinum occur but are rare. Diagnosis The diagnosis of asthma is made principally on clinical grounds and laboratory data are utilized in a supplementary or confirmatory fashion. A history of episodic wheezing in a nonsmoking patient, with findings of wheezing on physical examination is strongly suggestive of asthma. 5.Serology Total IgE is frequently elevated in serum in asthmatics. 6.Hematology Blood counts may reveal evidence of eosinophilia, which is usually mild, representing 5%-15% of the differential count. Profound eosinophilia (25% or greater, 3000 per ul or greater) should suggest another cause. Staging: The 4 stages of status asthmaticus are based on ABG progressions in status asthma. Patients in stage 1 or 2 may be admitted to the hospital, depending on the severity of their dyspnea, their ability to use accessory muscles, and their PEF values or FEV1 after treatment (>50% but <70% of predicted values). Patients with ABG determinations characteristic of stages 3 and 4 require admission to the ICU. The PEF value or FEV1 is less than 50% of the predicted value after treatment. Stage 1 -Patients not hypoxemic, but they are hyperventilating and have a normal PO2. -Recent data suggest that to possibly facilitate hospital discharge, these patients may benefit from ipratropium treatment via a handheld nebulizer in the emergency setting as an adjunct to beta-agonists. Stage 2 This stage is similar to stage 1, but patients are hyperventilating and hypoxemic. Such patients may still be discharged from the emergency department, depending on their response to bronchodilator treatment, but will require systemic corticosteroids. Stage 3 -These patients are generally ill and have a normal PCO2 due to respiratory muscle fatigue. -Their PCO2 is considered a false-normal value and is a very serious sign of fatigue that signals a need for expanded care. -This is generally an indication for elective intubation and mechanical ventilation, and these patients require admission to the ICU. -Parenteral corticosteroids are indicated, as is continued aggressive use of an inhaled beta2-adrenergic bronchodilator. -These patients may benefit from theophylline. Stage 4 This is a very serious stage marked by -PO2 is low (hypoxia) and PCO2 is high (hypercapnea) signifying respiratory failure. -Less than 20% lung function or FEV1 -Patients require intubation and mechanical ventilation. -Patients in stage 4 should be admitted to the ICU. -Switching from inhaled beta-2 agonists and anticholinergics to metered-dose inhalers (MDIs) via mechanical ventilator tubing is indicated. -Parenteral steroids are essential, and theophylline may be added, as with patients in stage 3. Monitoring: -Severe asthmatics should be monitored for heart rate, blood pressure, O2 saturation, and arterial pH and PaCO2. -Ventilator monitoring must be meticulous, because increases in peak inspiratory pressure or decreases in pulmonary compliance may signal worsening bronchoconstriction or an extrapleural air leak. Other definitions of asthma Near fatal asthma Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures 223mmHg Life threatening asthma –Stage 4 Any one of the following in a patient with severe asthma: 1- PEF <33% best or predicted 2- SpO2 <92% - PaO2 <8 kPa 3-Raised Pco2- normal PaCO2 (4.6 – 6.0 kPa) 4-Silent chest 5-Cyanosis 6-Feeble respiratory effort-with exhaustion- 7-Hypoventilation 8-Bradycardia and Dysrhythmia 9-Hypotension 10-Confusion, irritability and anxiety 11-Coma Acute severe asthma Any one of:-Stage 3 - PEF 33-50% best or predicted - respiratory rate ≥25/min - heart rate ≥110/min - inability to complete sentences in one breath Moderate asthma exacerbation - Increasing symptoms - PEF >50-75% best or predicted - no features of acute severe asthma Brittle asthma - Type 1: wide PEF variability (>40% diurnal variation for >50% of the time over a period >150 days) despite intense therapy - Type 2: sudden severe attacks on a background of apparently well controlled asthma Complications Complications of asthma include § Exhaustion § Dehydration § airway infection § cor pulmonale § tussive syncope § Pneumothorax occurs but is rare § Acute hypercapnic and hypoxic respiratory failure occurs in severe disease.

Late inflammatory response Release of inflammatory mediators prime adhesion molecules in the airway epithelium and capillary endothelium, which then allows inflammatory cells, such as eosinophils, neutrophils, and basophils, to attach to the epithelium and endothelium and subsequently migrate into the tissues of the airway. Eosinophils release eosinophilic cationic protein (ECP) and major basic protein (MBP). Both ECP and MBP induce desquamation of the airway epithelium and expose nerve endings. This interaction promotes further airway hyperresponsiveness in asthma. The 2 phases of asthma lead to:a ü increased airway resistance and obstruction. ü Air trapping results in lung hyperinflation ü Ventilation/perfusion (V/Q) mismatch ü Increased dead space ventilation. ü Decreased compliance and increased work of breathing. -The increased pleural and intra-alveolar pressures that result from obstruction and hyperinflation, together with the mechanical forces of the distended alveoli, eventually lead to a decrease in alveolar perfusion. -The combination of atelectasis and decreased perfusion leads to V/Q mismatch within lung units. The V/Q mismatch and resultant hypoxemia trigger an increase in minute ventilation. The early stages of acute asthma, hyperventilation may result in respiratory alkalosis but later respiratory acidosis occurs V/Q mismatch. Sex: In infants, males generally have more severe disease than females. In older children, males and females are equally affected. Asthma has a higher incidence among adult females. Age: Asthma is well distributed among people of all age groups. Children who have asthma in the first year of life and those aged 9-16 years tend to have much more severe disease. DDx -Pulmonary Hypertension, Primary -Congestive heart failure- Orthopnea, moist basilar rales, gallop rhythms, blood-tinged sputum -Croup -Stridor -Upper airway obstruction -Foreign-body aspiration -Neoplasm -Bronchial stenosis. -Recurrent episodes of bronchospasm can occur with carcinoid tumors -Recurrent pulmonary emboli - Chronic bronchitis - Eosinophilic pneumonias are often associated with asthmatic symptoms, as are various chemical pneumonias and exposures to insecticides and cholinergic drugs. -Bronchospasm occasionally is a manifestation of systemic vasculitis with pulmonary involvement. INVESTIGATIONS 1-Spirometry -The diagnosis of asthma is established by demonstrating reversible airway obstruction. -The evaluation for asthma should include spirometry (FEV1, FVC, FEV1/FVC) before and after the administration of a short-acting bronchodilator. -Reversibility is traditionally defined as a 15% or greater increase in FEV1 after two puffs of a b-adrenergic agonist -In severe airflow obstruction with significant air trapping, the FVC may also be reduced, resulting in a pattern that suggests a restrictive ventilatory defect. -Airflow obstruction is indicated by a reduced FEV1/FVC ratio (< 75%). -Peak expiratory flow (PEF) meters are handheld devices designed as monitoring tools to be used at home. - PEF monitoring can establish peak flow variability and assist in the determination of asthma severity in patients with asthma symptoms and normal spirometry. - PEF is generally lowest on first awakening and highest several hours before the midpoint of the waking day (diurnal variation). -Ideally, PEF should be measured in the morning before the administration of a bronchodilator and in the afternoon after taking a bronchodilator; 20% variability in PEF values from morning to afternoon or over time suggests asthma. Predicted values for PEF vary with gender, age, and height. 2- Arterial blood gases -During moderately severe exacerbations pulse oximetry may be of value. -During severe exacerbations arterial blood gases are indicated. -Hypoxemia is a frequent finding in this setting and is caused by a mismatch of ventilation and perfusion associated with bronchoconstriction, with a resultant increase in the alveolar-arterial oxygen difference. -Mild to moderate obstruction hyperventilate , and thus the arterial PCO2 is decreased -During prolonged and severe episodes respiratory muscle fatigue and the PCO2 may normalize or become elevated. A normal PCO2 during a severe exacerbation of asthma is thought to be an ominous sign, suggesting impending respiratory failure. Early intubation is recommended to avoid profound respiratory muscle fatigue or respiratory arrest. 3-Chest X-ray Hyperinflation of the lung may be present during severe exacerbations, Complications of their disease such as pneumonia, pneumothorax, or pneumomediastinum. Infiltrates may be seen in allergic bronchopulmonary aspergillosis. 4-Sputum examination Usually reveal inflammatory cells, including neutrophils and eosinophils, in the sputum of asthmatics, although this finding is of little diagnostic value. MANAGEMENT 1.Oxygen therapy -Administered via a nasal canula or mask. -With the advent of pulse oximetry, oxygen therapy can be easily titrated to maintain the patient's oxygen saturation above 92% (>95% in pregnant patients or those with cardiac disease). 2.Beta-2 Adrenergic agonists -The first line of therapy is bronchodilator treatment with a beta-2 agonist, typically albuterol. -Nebulizer treatments may be administered either continuously (10-15 mg/h) or by frequent timing (eg, q5-20min), depending on the severity of the bronchospasm. -The dose of albuterol for intermittent dosing is 0.3-0.5 mL of a 0.5% formulation mixed with 2.5 mL water for injection NB. Patients resistant to beta-2 agonists may be given nonselective beta-2 agonists (eg, epinephrine [0.3-0.5 mg] or terbutaline [0.25 mg]) administered subcutaneously. 3.Ipratropium bromide treatment -Ipratropium, can be synergistic with albuterol or other beta-2 agonists. -Ipratropium is administered every 4-6 hours. -Because children appear to have more cholinergic receptors, they are more responsive to parasympathetic stimulation than adults 4.Glucocorticosteroids Steroids are the most important treatment for status asthmaticus. The usual dose is oral prednisone at 1-2 mg/kg/d. Methylprednisolone provides excellent efficacy when given intravenously at 1 mg/kg/dose every 6 hours Loading dose: 125-250 mg IV Maintenance dose: 4 mg/kg/d IV divided q4-6h 5.Fluid replacement Intravenous fluids are administered to restore euvolemia. 6.Aminophylline -Conflicting reports on the efficacy of aminophylline therapy have made it controversial. -Starting intravenous aminophylline may be reasonable in patients who do not respond to medical treatment with bronchodilators, oxygen, corticosteroids, and intravenous fluids within 24 hours. -Recent data suggest that aminophylline may have an anti-inflammatory effect in addition to its bronchodilator properties. -The loading dose is usually 5-6 mg/kg, followed by a continuous infusion of 0.5-0.9 mg/kg/h. 6.Antibiotics The routine administration of antibiotics is discouraged. Patients are administered antibiotics only when they show evidence of infection (eg, pneumonia, sinusitis). DDX Upper airway disorders that mimic asthma include § vocal cord paralysis § vocal cord dysfunction syndrome § foreign body aspiration § laryngotracheal masses § Tracheal narrowing § Tracheomalacia § Airway edema as in the setting of angioedema or inhalation injury. Lower airway disorders include § Nonasthmatic chronic obstructive pulmonary disease (chronic bronchitis or emphysema), bronchiectasis § Allergic bronchopulmonary mycosis § Cystic fibrosis § Eosinophilic pneumonia § Bronchiolitis obliterane § Systemic vasculitides that often have an asthmatic component include Churg-Strauss syndrome and other systemic vasculitides with pulmonary involvement.