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Cerebral Palsy clinical findings

Vesicoureteric reflux (VUR): Pathogenesis and clinical findings

Vesicoureteric reflux (VUR): Pathogenesis and clinical findings Authors: Nicola Adderley Reviewers: Emily Ryznar *Lindsay Long * MD at time of publication Abnormal function Abnormal anatomy Neurogenic bladder (e.g. cerebral palsy, constipation, spinal injury, iatrogenic) Non-neurogenic bladder (neuropsychological) Lower urinary tract abnormality (posterior urethral valves, meatal stenosis) Bladder outlet obstruction ↑ pressure distorts UVJ Upper urinary tract abnormality (ureters) UVJ abnormality Incomplete closure of UVJ during bladder contraction Abbreviations • UVJ - ureterovesicular junction • UTI – urinary tract infection Failure of bladder sphincter to relax during bladder contraction Vesicoureteric reflux (VUR): Back flow of urine from the bladder into one or both ureters +/- kidneys Migration of lower urinary tract bacteria to kidneys Bacterial invasion of renal parenchyma Upper UTI (pyelonephritis) Incomplete emptying of bladder during Abnormal ↑ pressure in bladder Bladder dilates Dilated bladder on U/S urination Bacteria in bladder are not cleared during urination voiding habits ↑ bladder capacity Renal scarring ↓ functional renal tissue *Chronic kidney disease (↓ GFR, hypertension, proteinuria) Flank tenderness Fever, dysuria, urgency, frequency Lower UTI (cystitis) Urinary stasis Cloudy, foul- smelling urine Urethral stricture Notes Urgency, dysuria, frequency • First febrile UTI in an infant should trigger a work-up for VUR • High likelihood of spontaneous resolution • *Late complication of severe VUR Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 19, 2018 on www.thecalgaryguide.com

intraventricular-hemorrhage-in-preterm-infants-clinical-findings-and-complications

Intraventricular hemorrhage (IVH) in preterm infants: Clinical findings and complications Authors: Alexa Scarcello Reviewers: Nicola Adderley, Emily Ryznar, Yan Yu*, Jennifer Unrau* * MD at time of publication Volpe Grading Grade I: germinal matrix hemorrhage with no or minimal IVH (<10% of ventricular area) Grade II: IVH (10-50% of ventricle) Grade III: IVH (>50% of ventricle; usually distends lateral ventricle) Grade IV/Intra-parenchymal echodensity (IPE): periventricular hemorrhagic infarction Inflammation/dysfunction of arachnoid villi ↓ absorption of CSF 2° to obstruction of arachnoid villi Communicating hydrocephalus (IVH grades II-IV) Venous congestion Venous infarction Periventricular hemorrhagic necrosis Destruction of periventricular motor tracts Cerebral palsy Rapid significant blood loss ↓ intravascular blood volume Hypotension ↓ bloodflow to the brain to support brain function Intraventricular Hemorrhage (IVH) hemorrhage in periventricular subependymal germinal matrix Ultrasound: blood in germinal matrix, ventricles, or cerebral parenchyma Sudden ↓ hematocrit Blood irritates contiguous structures Variable neurologic findings; including altered level of consciousness, hypotonia, apnea, etc Neuro- developmental abnormalities (varying severity) See slide - Hydrocephalus: Clinical Findings in Pediatrics This mechanism leads to three different possible clinical manifestations: 1. Silent Presentation (most common) 2. Stuttering/Saltatory Course: non-specific findings - hypotonia, apnea, altered level of consciousness, bradycardia, and ↓ Spontaneous movements 3. Catastrophic Deterioration (least common) Stupor or coma, decerebrate posturing, seizures, bradycardia, metabolic acidosis, bulging fontanelles, abnormal pupillary reflexes, inappropriate ADH secretion Notes • Incidence & severity are inversely proportional to gestational age • 50% occur within 1st day of life, 90% by 3rd day • As explained in the flow chart, the postnatal clinical presentations of IVH fall into three categories (1-3) • Symptoms of catastrophic bleeds are uncommon and usually caused by rapid significant blood loss with subsequent neurologic findings 2° to meningeal irritation, inflammation, and potential mass effect/acute hydrocephalus; severe bleeds may also occur in the absence of clinical findings attributable to IVH Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 27, 2019 on www.thecalgaryguide.com

Epilepsy Pathogenesis

Epilepsy: Pathogenesis Genetic susceptibility Angelman syndrome, Fragile X syndrome, Tuberous sclerosis, neurofibromatosis Chromosomal abnormalities cause abnormal neural patterns Neural Cerebral palsy, focal cortical dysplasia Malformation of cortical development Cerebrovascular Intracranial hemorrhage, ischemic stroke Other Acquired Head trauma, cerebral infection (i.e., HSV1, VZV, cysticercosis) Neoplasm Metabolic Inborn errors of metabolism Inherited enzyme deficiencies Neurodegenerative Alzheimer’s Disease Protein-rich plaque build-up and brain atrophy Inflammation and formation of scar tissue irritates neural tissue Infiltration of mass, grey matter irritation Damage to the brain and subsequent alteration of neuronal circuitry Neurotransmitter imbalances (i.e. ↑ glutamate, ↓ GABA, ↓ serotonin, ↓ dopamine, ↓ noradrenaline) Abbreviations: • HSV1 – Herpes Simplex Virus 1 • VZV – Varicella Zoster Virus ↑ Inflammatory cytokines (e.g. interleukin-6, tumor necrosis factor-α) Altered neurogenesis and gliosis Ion channel and receptor dysfunction causes imbalance of ion channel charges Authors: Keerthana Pasumarthi Christopher Li Reviewers: Negar Tehrani, Ephrem Zewdie, Ran (Marissa) Zhang, Carlos R. Camara-Lemarroy* * MD at time of publication Neurons fire in burst activity (referred to as paroxysmal depolarization shift) and often in groups (hypersynchrony) Abnormal neural activities eventually create self-reinforcing circuits and transform neural network over time Injuries from falls, bumps, operating heavy machinery Involuntary contractions Loss of consciousness Post-ictal confusion Recurrent seizures Sudden Unexplained Death of Epilepsy Patient (SUDEP) Loss of airway reflexes Aspiration of saliva or food contents Aspiration Pneumonia Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published July 5, 2022 on www.thecalgaryguide.com

Dantrolene

Dantrolene: Mechanism of Action and Adverse Side Effects Medication indicated for the treatment of muscle spasms associated with malignant hyperthermia (reaction to certain anesthetics resulting in a rapid and dangerous increase in body temperature, muscle rigidity, and other symptoms), and spasticity associated with various neurological disorders such as multiple sclerosis, cerebral palsy, and spinal cord injury. Dantrolene Authors: Madison Amyotte, Arzina Jaffer Reviewers: Jasleen Brar, Mao Ding Luiza Radu Joanna Moser* * MD at time of publication Metabolized in the liver by the cytochrome P450 enzyme Metabolic process forms a high concentration of hydroxylamine Hydroxylamine is a highly toxic metabolite associated with dantrolene induced liver injury Impaired Liver Function Binds to ryanodine receptors (RYR1) in the sarcoplasmic reticulum of skeletal muscle cells Prevents ryanodine channel from opening when triggered by the action potential in the muscle Prevents calcium release from the sarcoplasmic reticulum Prevents binding of calcium to troponin on the actin filaments in the cytosol of the skeletal muscle cells Myosin-binding site on the actin remains covered by the tropomyosin Prevents cross-bridge formation between myosin and actin within the sarcomere Prevents muscle contraction ↓ Progression of muscle rigidity and spasms ↓ Heat produced by muscular contraction Skeletal & respiratory muscle weakness ↓ Body temperature ↓ Inspiratory capacity Dyspnea Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Feb 18, 2024 on www.thecalgaryguide.com

Fetal Complications of Labour and Vaginal Delivery

Fetal complications of labour and vaginal delivery Fetus passing through cervix and birth canal puts pressure and physical stress on the head Labour/vaginal delivery Fetus is not presented head- first in the vaginal canal (e.g. breech, shoulder, transverse) Abnormal positioning increases risk of umbilical cord becoming entangled or dropping in front of the fetus in the birth canal Passage of the fetus through birth canal compresses the umbilical cord Edema Perinatal hypoxia Signs of fetal distress (e.g. late decelerations, changes in fetal heart rate, ↓ fetal movement) Infant death Uterine contractions are too weak to progress labour Prolonged time in labour results in increased total number of contractions Fractures (most commonly affecting the clavicle) Uterine contractions compress blood vessels in the placenta, resulting in reduced blood flow Severe obstetric hemorrhage causes circulating blood flow to decrease as blood volume is lost (see relevant slide for pathogenesis) Small birth canal to baby size ratio Lack of space traps the fetal shoulders following delivery of the head (shoulder dystocia) Excessive lateral traction or stretching damages nerves in the brachial plexus Erb’s palsy (paralysis of the arm caused by injury to C5-C6 of the brachial plexus) Shearing force on the skull and scalp ruptures blood vessels Cephalohematoma (blood accumulation below periosteum) Boggy, soft lump on infant’s head Soft tissue injury triggers release of inflammatory signaling molecules, which ↑ vascular permeability Caput succedaneum (scalp swelling) Boggy, soft swelling of infant’s head that extends across suture lines Mild soft tissue injury Hypoxic ischemic encephalopathy Variable signs of brain injury: seizures, hypotonia, difficulty feeding, etc. Cerebral palsy Developmental delay, hypotonia, spasticity, etc. Authors: Jasmine Nguyen Reviewers: Akanksha Bhargava Michelle J. Chen Sarah Glaze* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Apr 29, 2024 on www.thecalgaryguide.com