Convulsions in Pregnancy PDF

Convulsions in pregnancy D.D of Convulsions in pregnancy? Directly related to pregnancy convulsions due to pregnancy ( eclampsia) convulsions aggregation by pregnancy ( Epilepsy) Not directly related to pregnancy CNS infection Trauma ( traumatic braininj...

Convulsions in pregnancy D.D of Convulsions in pregnancy? Directly related to pregnancy convulsions due to pregnancy ( eclampsia) convulsions aggregation by pregnancy ( Epilepsy) Not directly related to pregnancy CNS infection Trauma ( traumatic braininjury ) tetany Drugs withdrawal Metabolic ( hyperglycemia - Hypoglycemia - hyponatremia - Hypocalcemia ) Mention criteria for diagnosis of each 1. Preeclampsia HTN more than 140/90 mmHg on two occasions at least 4 hours apart proteinuria > 300mg in 24-hours in patients at 20 weeks gestation 2. Eclampsia as Preeclampsia + Tonic clonic seizures 3. Epilepsy Occurring anytime during pregnancy known case of epilepsy no Hx of HTN and proteinuria Eclampsia Epilepsy Occur after 20 weeks Occur anytime during of pregnancy pregnancy Preeclampsia Previous Epileptic fits induced hypertension Tonic clonic No Hx of HTN and convulsion proteinuria HTN - proteinuria - edema - pulmonary edema C/P of eclampsia elevated BP - swelling in the face and hand - headache - excessive weight gain - Nausea and vomiting - vision problems - difficult in urination - Abdominal pain RUQ C/P of Epilepsy uncontrolled jerky movement of arm and legs - loss of consciousness - temporary confusion - psychic symptoms ( fear, anxiety , deja vu ) - panic attack Investigation Eclampsia : CBC - liver enzymes - HELLP syndrome ( hemolysis - elevated liver enzymes - low Platelets ) Epilepsy : ECG – EEG – MRI Maternal complications of eclampsia injury tongue acute renal failure pulmonary embolism liver failure or hge aspiration pneumonitis cerebral hge post Mortem collapse Neonatal complication preterm delivery IUGR hypoxic - neurologic injury perinatal death - long term CVS morbidity Coma Mental status = content ( cerebral hemispheres ) + arousal ( ARAS) Altered mental status Change in arousal : lethargy - stupor - coma Change in content : ( simple changes " speech - calculations - spelling " ) ( complex changes " emotions – behavior - personality " ) Definition of levels of arousal ( consciousness ) Alert ( conscious ) : appearance of wakefulness Lethargy : Mild reduction in alertness ( subconscious ) Obtundation : Moderate reduction in alertness ‫مش هيرد عليك ع طول‬ Stupor : deep sleep ( response to painful stimuli) Coma ( unconscious ) sleep like appearance and behavior unresponsive to all external stimuli Psychologenic unresponsiveness ( common cause of coma in ER ) Patient apparently unconscious usually shows some response to external stimuli Elicit the corneal reflex may cause a vigorous contraction of the orbicularis oculi Marked resistance to passive movement of the limbs may be present Define coma patients out true content with environment and other people / state of unconsciousness in which the eyes are closed and sleep wake cycles absent Common causes of Coma Toxins - Metabolic disorders - partial complex seizures - head trauma - Acute febrile systemic illness GCS motor "M" ( obey command - localized to pain - withdrawal from pain - flexion in response to pain - extension to pain - no motor response ▶️verbal "V " ( oriented - confused - inappropriate words - incomprehensible sound - none ) ▶️eye "E" ( Open spontaneous - open to verbal - open to pain – no opening 7.30 ‫ مثال عند الساعه‬M 3 V2 E2 ‫ بنكتب مثال‬GCS ‫لما بنيجي نكتب ال‬ Minor >13 ⚡ moderate 9-13 ⚡ severe < 8 Approach to coma patients General examination 👉ABCDE - IV access + estimate blood glucose level and other biochemical parameters , drugs screening Assessment of the patient - severity of the coma - diagnostic evaluation Take information from ( relatives - paramedics - ambulance personal ) Previous medical Hx ( Epilepsy - DM – drug history ) Clues obtained from the patient ( clothing or handbag ) Ex for trauma and log roll to examine the back , needle marks Vital sign Hypothermia 👉 hypopituitarism - hypothyroidism - chlorpromazine ( exposure to low temperature) ⚡ Generalized Rigidity and muscle fasciculation ( hypoxia and hypercapnia are common ) ⚡ treatment " gradual warming and may require Peritoneal dialysis with warm fluid Hyperthermia ( febrile coma ) 👉 CNS infection 1st / pontine Hge / SAH / thyrotoxic - Addison crisis / salicylate poisoning / sun stroke , heat stroke / coma to 2nd infection " UTI , pneumonia , tetanus " 2nd Bradycardia 👉 brain tumors - opiates - myxodema Tachycardia 👉 hyperthyroidism - Uremia High blood pressure 👉 HTN encephalopathy Low blood pressure 👉 Addison crisis - Alcohol - barbiturate ▶️respiration 1. Cheyne stokes respiration ( hyperpnea alternates with apnea ) 👉 common in cerebral disease - acidosis - pneumonia 2. Apneustic breathing 👉 pons lesions ( pause at full inspiration ) 3. Ataxic 👉 medullary lesions ( irregular respiration with random deep and shallow breath 4. Central neurologenic 👉 M.B lesions Odor of breathin 1. Acetone ( DKA ) 2. Fetor hepatic ( hepatic coma) 3. Urine ferous Odor ( uremic coma) 4. Alcohol Odor ( alcohol Intoxicantion) Skin ▶️ injury and bruises ( traumatic causes) ⚡ dry skin ( DKA – Atropine ) ⚡ moist skin ( Hypoglycemic Coma) ⚡cherry red ( co poisoning) ⚡ needle marks ( addiction) ⚡ rash ( meningitis- endocarditis) Pupils dilated ( Atropine ) Pupil constrict ( opiate - pontine Hge - organophosphatase ) ‫ دا نديله‬organophosphatase ‫ دقيقه دا ميت عيان ال‬١٥ ‫ اكتر من‬dilated fixed Pupil ‫لو‬ Atropine How to evaluate conscious level GCS – AVPU- Pupillary response random blood glucose ‫ اول حاجه نعملها ليه هى‬coma ‫عيان جايلك ب‬ Hypoglycemic Coma 👉 random glucose < 45 - confused, Comatose - rapid response to dextrose within 1-2 minutes Hypoglycemic status 👉 random glucose >45 - not response to dextrose Causes OF Coma CNS Causes 👉 head injury - cerebrovascular disease - HTN encephalopathy - raised ICP – infection Metabolic disorders ( hepatic , renal , endocrine , disturbance glucose level ) Miscellaneous Causes ( seizures - drugs - eclampsia - disturbance of ca and mg metabolism ) 1. Stroke ( mechanis " impairment of perfusion of the RAS with hypotension , Brian stem herniation ( parenchymal Hge ) 2. Hepatic coma ( how to Diagnosis) pts is known to be suffering from liver failure Sign of decompensated liver disease ( jaundice - Palmar erythema - ascites - LL edema - Parotid enlarged ) Asterixis ( flapping tremors ) Precipitating F ( git bleeding - infection - diuretic - sedatives – analgesia - anesthesia - high protein diet ) EEG with paroxysms of bilateral synchronous slow waves in delta range with occasional triphasic waves Stages ( Stage 1 – personality changes / Stage 2 – lethargy , flapping tremors , muscle twitches / Stages 3 – Nagy , abusive , violent / Stage 4 – coma ) Treatment ( colonic wash and treated RF) 3. Renal coma ( occur in acute or chronic RF - raised blood urea - Metabolic acidosis - electrolyte disturbance and water intoxication ⚡ early symptoms " headache – vomiting - Dyspnea - mental confusion - insomnia / later muscular twitching - Asterixis ⚡ increase blood urea and creatinine 4. Dialysis disequilibrium syndrome ( …. 5. Dialysis encephalopath ( … 6. DKA (subacute onset - marked ketoacidosis above 40 mmol /l - secondary lactic acidosis - patients are dehydrated - plantar responses ) DM type 1 - children 14 Ttt 👉 insulin + K + fluid 6L in 1st 6h - antibiotics 7. Hyperglycemia non ketotic diabetic coma ( elderly - profound cellular dehydration risk of developing cerebral venous thrombosis - random >600 - high osmolarity > 315 - type 2 DM ⚡ May be induced by drug , acute Pancreatitis , burn , and heat stroke ) TTT 👉 fluid - insulin - anticoagulant 8. Hypoglycemic Com ( mush more rapid onset and complications / symptoms appear with blood sugar of less than 445 mg / dl Diagnosis 👉 Hx of taking insulin or spontaneous Hypoglycemia with insulinoma / symptoms related to Fasting or exercise / may precipitating by hepatic disease , alcohol intake - hypopituitarism - Addison disease Ttt 👉 coma cocktail 9. Poisoning , drugs abuse and alcohol Intoxicantion ( 80% require simple observation) Most common drugs ( benzodiazepines - paracetamol - antidepressants - heroin Coma easy reversible with naloxone 0.4mg bolus and repeated dos Investigation of coma 👉 blood will be taken for determination of glucose , Electrolytes, liver function , ca , osmolarity , blood gases / CT scan / LP / ECG / EEG  Coma cocktail 👉 dextrose 50 - naloxone - thiamine - flumazenil Causes of urgent dialysis 👉 Uremic coma - severe Metabolic acidosis ph 0.4 ng/mL, or Troponin T > 0.1 ng/mL Pulmonary Infarction Syndrome: Ccause by a tiny peripheral Pulmonary artery embolism Symptoms: Pleuritic chest pain Low-grade fever leukocytosis Pleural rub Hemoptysis Differential Diagnosis (D.D.) of PE 《 Dyspnea + chest pain 》 USA, MI, CHF, Pneumothorax, Asthma ,Bronchitis Investigations: CXR / D-dimer / ECG / ECHO / Pulse oximetry / ABG CT angiography = most accurate CXR findings " normal study in 24% of cases " 《 Hampton’s hump (wedge-shaped) Westermark sign Atelectatic band chronic infection - chronic fibrosis ‫ عندنا ال‬fibrotic band ‫ايه الحاجات الل ممكن تعمل‬ - PE – Bronchoctesis ECG findings Help to exclude Acute MI 《 RBBB Inverted T wave in Leads V1-V4 S1Q3T3 P pulmonale ST depression in V6 》 Echo ( limit accuracy.. ABG findings 《 Hypoxemia Hypocapnia 》 Pulmonary angiogram Troponin Doppler US of leg vein BNP – pro BNP > 500Pg /ML CT angiography 《 Better sensitivity & specificity 》 D-dimer 《 Good negative test 》 Quantitative test (ELISA) have 80-85% sensitivity, and 93-100% negative predictive value & but low specificity, Positive assay is 500 ng/ml. Qualitative (RBC agglutination test); less sensitive. False Positives Pregnant Patients Post-partum < 1 week Malignancy Surgery within 1 wee Advanced age > 80 years Sepsis Hemorrhage CVA AMI Collagen Vascular Diseases Hepatic Impairment Approach to the patient of PE Diagnosis by S&S + risk factor D-dimer ( if negative = not PE ) 《 D-dimer Positive according to stability ( CTA – Echo ) If unstable ( Echo ) according to RV strain if present give Thrombolytic ) Treatment goals Prevent death - minimize the long-term morbidity - reduce the likelihood of recurrence embolic events Treatment options for pulmonary emboli: Anticoagulation. Inferior vena cava filter. Additional options for massive PE: Thrombolytic agent. ( hemodynamic compromise - pulmonary HTN OR Rt side ventricular dysfunction detect by Echo ) Catheter embolectomy. Surgical embolectomy. Haemodynamic support – inotropes. Acute abdominal pain with pregnancy 2. A 22-year-old newly married woman comes to the emergency unit complaining of bilateral severe lower abdominal pain, abnormal vaginal bleeding and offensive vaginal discharge. Her temperature was 39. On bimanual vaginal examination, there is adnexal tenderness and cervical motion tenderness. The pregnancy test was positive. 1. What is the DD for this case. Ectopic pregnancy Rupture / abortion ( septic) Pelvic inflammatory disease Ovarian abscess - tubal abscess 2. What is the most probable diagnosis. Rupture ectopic pregnancy / septic abortion 3. Investigation CBC - CRP , ESR / blood culture & vaginal culture Trans-vaginal U/S Beta HCG 4. What are the possible aetiologic agents. Previous Hx of ectopic pregnancy / recurrent ectopic pregnancy PID IUD Hx of Pelvic surgery 5. How can you manage this case. Assessment Resuscitation ( IV fluids – blood transfusion ) Analgesia - antibiotics Obstetrics consultants 6. what are the possible future complications if left untreated. hemorrhage / PID DIC / Septic shock Pelvic abscess Death Acute abdominal in pregnancy  Hx :pain ( associated symptoms 《 vaginal bleeding - Preeclampsia symptoms 《 obs Hx [ LMP – number of gravid and parity , confirm any contraceptive 》 Physical examination 《 general ( ABCDE ) – abdominal - assessment pregnancy and uterus 》 Investigation pregnancy test - CBC – LFT – RFT – urine analysis - MRI – Laparoscopic + biopsy CT ( non pregnant ) Trans-vaginal U S - trans abdominal US D.D of abdominal pain during pregnancy Neurological emergency Head trauma : describe external trauma to craniofacial area from various causes Head injury : clinical evidence injury on physical examination ( ecchymosis – laceration ) TBI : injury to brain parenchyma as a result trauma Common Etiology MVC – falls - assault - sporting injury Blunt > penetrate injury ‫ منهم بسبب‬%75‫ سنه و‬14 ‫ بيكون تلتهم اطفال تحت‬HT ‫ سنوي من ال‬ER ‫مليون ونص بيدخل ال‬ falls and MVC Types , mechanism open / closed Blunt / Penetrating accelerated / decelerated coup / contracoup Sites of injury Scalp : laceration - subgaleal hematoma Skull : open or closed fracture - linear - Depressed - basilar F Brain : 1ry or 2nd Intracranial vascula : EDH - SDH – SAH – ICH  according to severity ( TBI ) Mild head injury 《 GCS 14-15 AVPU alert or response to voice 》 Moderate head injury 》GCS 9-13 AVPU response to pain 》 Severe head injury 《 GCS 3-8 AVPU unresponse 》  Mild symptoms loss of consciousness - headache and N/V – fatigue - dizziness - difficult sleeping - speech problems moderate symptoms loss of consciousness - repeated vomiting or Nausea - convulsions - seizures - dilated one or both pupils of eyes - inability to awaken from sleep - weakness or numbness - loss of coordination or balance - irregular breathing - difficult speaking Indications for Hospital Referral Any of the following: Impaired consciousness level at any time Antero or retrograde amnesia Neurological symptoms (seizure, headache, vomiting) Clinical evidence of a skull fracture (e.g. CSF leak, periorbital hematoma) Significant extracranial injuries Worrying mechanism (e.g. high energy), possible penetrating injury) Uncertain diagnosis after first assessment Med comorbidity (anticoagulant use, alcohol abuse) Adverse social factors (e.g. alone, evidence of domestic violence Investigation 《 CT 》 identify brain injury , intracranial hematoma Indication in 1 hours 《 GCS 65 y with coagulopathy including drugs 《 within 8h ( amnesia > 30 minutes before event What are the objectives of management in TBI Initia resuscitation & management Prevention of secondary insult 《 hypoxia - aspiration - hypovolemia - Hypoglycemia – convulsions 》 Treating complications initial management 《 ABCDE 》 Clear and Maintain Airway + provide O2 as required & protect cervical spine Check and support breathing Check BMG and treat Hypoglycemia if present Insert two large IV cannulae send blood for cross match , FBC , Clotting screen Correct hypovolemia ,resuscitation If GCS 7 mmol Causes 1. Cellular shift : acidosis , drug like Bb , digitalis 2. Exogenous source; oral k replacement 3. Endogenous source; sever tissue damage 4. Some disease Manifestation Asymptomatic Weakness, irritable muscle Arrthymaia ECG : tall T wave , prolonged PR interval Treatment 1. Ca chloride 10mg or Ca clugonate 30 mg 2. B agonist 3. 10 U of Insulin with 50 ml 50% glucose 4. Remove k by diuretic or Resin 5. Hemolysis in severe hyperkalemia Sodium 《 Normal level 135- 145 mmol /l 》 Hypenatemia is the most common electrolytes disorder Causes 1. Excess free water administration 2. Any stress : surgery, tumor 3. Hyper osmolar hyponatremia (common cause) 4. urinary excretions: diuretic Manifestation Majority: asymptomatic Symptom develop when Na 5 min or repeated seizures with NO regain in consciousness. Aura, ictus, postictal….interictal 🪟 Etiology Idiopathic (most common) MCQ Symptomatic → congenital anomalies / CNS / meningitis / electrolytes disturbance 🪟 Causes of seizures Epilepsy 《 Idiopathic (70-80%) MCQ 》 Secondary to Cerebral malformation Cerebral vascular occlusion Encephalopathy Ischemia Cerebral tumor Neurodegenerative disorder Non-epileptic causes exclude: Febrile convulsion Metabolic → hypoglycemia / hypocalcemia / hypo magnesaemia / hypo- hypernatremia Head trauma Meningitis - Encephalitis Toxins 🪟Diagnosis History 《 Diagnosis Epilepsy primary depends on detailed history from child and eyewitness or by video if available 》 particular attention is focused on any specific trigger ( educational - psychological or social problems ) Clinical Examination includes skin markers for neurocutaneous $ or neurological abnormality 🪟 Investigation Platelets - smear AEDs CBC / Ca⁺ / PO₄ / Glucose / Electrolytes / Liver function EEG ( regular , sleep deprived , videotape ) CT / CSF (not routine 1mm New Q waves Any ST-E New Conduction Defect New ST-D NORMAL ECG ‫ اعيده تانى كمان ساعتين‬Chest pain ‫ وفيه‬Normal ECG ‫ لقيت‬ACS ‫لو لقيت مع‬ ‫ ف اول مره‬%50 ‫ بيشخص‬ECG ‫ال‬ % ٨٠ ‫وتانى مره لحد‬ STEMI ST elevation >2 lead - hyperacute T wave followed by T wave inversion ( NACB) Task for the Redefinition of Myocardial Infarction Cardiac troponin is the preferred marker for the diagnosis of MI and for risk stratification. CK-MB by mass assay is an acceptable alternative when troponin in not available. CK-MB was preferred for the detection of reinfarction early increased sensitivity and specificity of cTn should make it the marker of choice it is unnecessary to obtain both values. Cardiac troponins I and T are equally useful. Non ACS cause of troponin elevation Trauma - CHF – AORTI valve disease - HTN - hypotension - renal failure - hypothyroidism - mayocarditis TIMI Risk Score T: Troponin elevation (or CK-MB elevation) H: History or CAD (>50% Stenosis) R: Risk Factors: > 3 (HTN, Hyperlipidemia, Family Hx, DM II, Active Smoker) E: ECG changes: ST elevation or depression 0.5 mm A2:Aspirin use within the past 7 days; Age over 65 T: Two or more episodes of CP within 24 hours Specifics of Early Hospital Care Anti-Ischemic Therapy Anti-Platelet Therapy Anticoagulant Therapy Early Hospital Care 《 Anti-Ischemic Therapy MONA-BAH 》 Bed rest and Telemetry with morphine Oxygen (maintain saturation >90%) Nitrates (SLx3 Oral/topical. IV for ongoing ischemia, heart failure, hypertension) Aspirin (162-325 mg), Clopidogrel for those with Aspirin allergy/intolerance (300-600 mg load and 75 mg/d Oral B-blockers in First 24-hours if no contraindications. (IV B-blockers class IIa indication) ACE inhibitors in first 24-hours for heart failure or EF