Birth Asphyxia and Hypoxic-Ischemic Encephalopathy — MCQs

10 questions

Which of the following is NOT an essential criterion for diagnosing perinatal asphyxia?

According to neonatal resuscitation protocol, how much oxygen to give in a term neonate with apnea and bradycardia initially?

Cells most sensitive to hypoxia are?

A preterm infant with poor respiration at birth starts throwing seizures at 10 hours after birth. Antiepileptic of choice shall be:

Burst suppression pattern on EEG is typically seen in:

Lendrum's stain is done for:

Which of the following anesthetic agents will produce decreased EEG activity?

A hyperventilating patient has the following ABG values: pH=7.53, pCO2=20 mmHg, HCO3= 26 mEq/L. What is the most likely diagnosis?

All of the following are true about Status marmoratus:

Q10

Which of the following is a key clinical feature of hypoxic ischemic encephalopathy?

Birth Asphyxia and Hypoxic-Ischemic Encephalopathy Indian Medical PG Practice Questions and MCQs

Question 1: Which of the following is NOT an essential criterion for diagnosing perinatal asphyxia?

A. Prolonged metabolic alkalosis (Correct Answer)
B. Hypoxic ischemic encephalopathy (HIE) in the immediate neonatal period
C. Evidence of multiorgan dysfunction in the immediate neonatal period
D. Persistence of Apgar score of 0-3 for >5 min

Explanation: ***Prolonged metabolic alkalosis*** - This is **NOT** an essential criterion for diagnosing perinatal asphyxia because asphyxia causes the opposite condition — **metabolic acidosis**, not alkalosis. - During oxygen deprivation, anaerobic metabolism produces lactic acid, leading to **acidosis** (low pH, high lactate). - **Metabolic alkalosis** (excess bicarbonate or loss of acids) is incompatible with the hypoxic-ischemic insult of asphyxia. *Persistence of Apgar score of 0-3 for >5 min* - A **persistently low Apgar score** (0-3 for more than 5 minutes) is a strong indicator of perinatal asphyxia and is one of the **essential criteria**. - It reflects severe cardiorespiratory depression and the infant's inability to establish effective breathing and circulation. *Hypoxic ischemic encephalopathy (HIE) in the immediate neonatal period* - The development of **HIE** is a direct and severe consequence of perinatal asphyxia, signifying brain damage due to lack of oxygen and blood flow. - This is a **critical diagnostic criterion**, as it indicates significant neurological impact from the asphyxial event. *Evidence of multiorgan dysfunction in the immediate neonatal period* - Asphyxia can lead to widespread tissue damage due to oxygen deprivation, affecting organs like the kidneys, heart, lungs, and liver, in addition to the brain. - **Multiorgan dysfunction** is a **key essential criterion** that supports the diagnosis of severe perinatal asphyxia.

Question 2: According to neonatal resuscitation protocol, how much oxygen to give in a term neonate with apnea and bradycardia initially?

A. 100%
B. 21% (Correct Answer)
C. 50%
D. 30%

Explanation: ***21%*** - According to **NRP (Neonatal Resuscitation Program) 2020 guidelines**, for **term neonates (≥35 weeks gestation)** requiring resuscitation, the initial recommendation is to use **room air (21% oxygen)** to minimize the risk of hyperoxia and oxidative injury. - Multiple randomized controlled trials have demonstrated that room air is as effective as 100% oxygen for initial resuscitation. - Supplemental oxygen is only added if **oxygen saturation targets** are not met despite adequate ventilation, and should be titrated using **pulse oximetry**. *30%* - This concentration is **higher than room air** and is not the initial recommendation for term neonates needing resuscitation. - Starting with a higher oxygen concentration can lead to **oxidative stress** without immediate benefit. - Higher initial concentrations (21-30%) are reserved for **preterm neonates (<35 weeks)**. *100%* - Administering **100% oxygen** can be harmful to a neonate, potentially causing **oxidative injury** to developing organs, including the lungs, brain, and retina. - This was the old practice but has been **discontinued** based on evidence showing increased mortality and morbidity. - High concentrations are no longer recommended even in severe cases; oxygen should be titrated to saturation targets. *50%* - While lower than 100%, 50% oxygen is still **not the initial recommended concentration** for term neonates in resuscitation protocols. - The goal is to start with **21% oxygen** and gradually increase based on **pulse oximetry monitoring** and target saturation ranges if 21% is insufficient.

Question 3: Cells most sensitive to hypoxia are?

A. Myocardial cells
B. Neurons (Correct Answer)
C. Hepatocytes
D. Renal tubular epithelial cells

Explanation: ***Neurons*** - Neurons have a very high metabolic rate and an **absolute requirement for oxygen** and glucose to maintain their complex electrochemical functions and ionic gradients. - Due to their lack of significant energy reserves and high metabolic demand, they can sustain **irreversible damage within minutes** (typically 3-5 minutes) of complete oxygen deprivation. *Myocardial cells* - While myocardial cells are highly susceptible to hypoxia and can undergo **ischemic necrosis** (e.g., in a myocardial infarction), they can often tolerate oxygen deprivation for somewhat longer periods than neurons due to some anaerobic metabolic capacity. - Significant damage to myocardial cells usually occurs after **20-30 minutes of severe ischemia**. *Hepatocytes* - Hepatocytes (liver cells) are relatively **resilient to hypoxia** compared to neurons, possessing significant metabolic flexibility and capacity for regeneration. - They can endure **longer periods of oxygen deprivation** before irreversible damage occurs, often hours. *Renal tubular epithelial cells* - Renal tubular epithelial cells are generally **sensitive to hypoxia**, especially those in the medulla, due to their high metabolic activity for reabsorption and secretion. - They are a common target for **acute tubular necrosis** in ischemic injury but generally have a **higher tolerance than neurons**, with damage becoming widespread after tens of minutes to an hour of severe ischemia.

Question 4: A preterm infant with poor respiration at birth starts throwing seizures at 10 hours after birth. Antiepileptic of choice shall be:

A. Phenobarbitone (Correct Answer)
B. Lorazepam
C. Levetiracetam
D. Phenytoin

Explanation: ***Phenobarbitone*** - **Phenobarbitone** is the **first-line antiepileptic drug** recommended for neonatal seizures due to its established efficacy and safety profile in this population. - It acts primarily by **potentiating GABAA receptor-mediated chloride currents**, leading to central nervous system depression and seizure control. *Lorazepam* - While **benzodiazepines** like lorazepam can be used for acute seizure cessation, especially status epilepticus, they are generally **not the first-line choice for maintenance therapy** due to potential sedation and respiratory depression in neonates. - Its short duration of action and risk of rebound seizures make it less suitable as a sole agent for ongoing seizure control. *Levetiracetam* - **Levetiracetam** is an increasingly common antiepileptic in neonates, but its long-term efficacy and safety, particularly regarding neurodevelopmental outcomes, are **still under investigation** compared to phenobarbitone. - While it may be used as a second-line agent or in specific situations, it is **not universally considered the first-line drug of choice** for neonatal seizures. *Phenytoin* - **Phenytoin** is typically considered a **second-line or third-line antiepileptic** for neonatal seizures, primarily used if phenobarbitone is ineffective. - Its use is limited by potential side effects such as **cardiac arrhythmias, hypotension, and infiltration at the injection site**, which can be particularly concerning in premature infants.

Question 5: Burst suppression pattern on EEG is typically seen in:

A. Absence seizures
B. SSPE
C. Herpes simplex encephalitis
D. Anoxic encephalopathy (Correct Answer)

Explanation: **Anoxic encephalopathy** - **Burst suppression pattern** on EEG, characterized by alternating periods of high-amplitude generalized slowing or sharp waves ("bursts") and periods of nearly flat line ("periods of suppression"), is a common finding in severe forms of **anoxic brain injury** and deep coma [2]. - This pattern indicates a severely dysfunctional brain, often with a **poor prognosis for neurological recovery** following cardiac arrest or other causes of cerebral anoxia [2]. *Absence seizures* - Characterized by **3-Hz generalized spike-and-wave discharges** on EEG [1], [3], which are distinct from burst suppression. - These seizures typically involve brief lapses of consciousness without significant motor activity and are not associated with diffuse brain damage leading to burst suppression [3]. *SSPE* - **Subacute sclerosing panencephalitis (SSPE)** due to chronic measles virus infection typically shows distinctive **periodic complexes** on EEG (Radermecker complexes), not burst suppression. - The disease has a progressive course with cognitive decline, myoclonus, and other neurological deficits. *Herpes simplex encephalitis* - Often characterized by **periodic lateralized epileptiform discharges (PLEDs)** on EEG, particularly over the temporal regions. - This pattern reflects the focal inflammation and neuronal damage caused by the HSV infection, which is localized and asymmetrical, unlike the generalized suppression seen in anoxic encephalopathy.

Question 6: Lendrum's stain is done for:

A. Air embolism
B. Pulmonary embolism
C. Fat embolism
D. Amniotic fluid embolism (Correct Answer)

Explanation: ***Amniotic fluid embolism*** - **Lendrum's stain** (MSB - Martius Scarlet Blue) is specifically used to identify **fibrin**, **mucin**, and **squamous cells** in the pulmonary vasculature, which are characteristic findings in amniotic fluid embolism. [1] - This stain excellently demonstrates **fibrin** (stains red) and helps visualize components of amniotic fluid that embolize to the mother's lungs, leading to a severe, often fatal, obstetric emergency. [1] - Lendrum's method is particularly valuable in forensic pathology and autopsy diagnosis of this condition. *Air embolism* - Air embolism diagnosis relies on identifying **air bubbles** in the cardiovascular system, often confirmed by imaging studies or direct visualization during autopsy. [1] - Special stains are not typically used for direct detection of air in tissue sections. *Pulmonary embolism* - Pulmonary embolism, typically caused by a **blood clot**, is diagnosed by identifying **fibrin** and **red blood cells** within pulmonary arteries, often with stains like hematoxylin and eosin (H&E). [1] - While Lendrum's stain can demonstrate fibrin, it is specifically employed when amniotic fluid embolism is suspected, not for routine thromboembolic disease. *Fat embolism* - **Fat embolism** is diagnosed by demonstrating **fat globules** in the pulmonary microvasculature using **fat stains** like **Oil Red O** or **Sudan Black**, usually on frozen sections. - Lendrum's stain does not specifically highlight fat emboli. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 322-324.

Question 7: Which of the following anesthetic agents will produce decreased EEG activity?

A. Ketamine
B. N2O (Correct Answer)
C. Thiopental
D. Propofol

Explanation: ***N2O*** - **Nitrous oxide (N2O)**, a volatile anesthetic, typically causes an **increase in EEG activity** or amplitude, rather than a decrease, particularly at subanesthetic concentrations, indicating cortical arousal. - It maintains **cerebral metabolic rate of oxygen consumption (CMRO2)** and cerebral blood flow (CBF) and does not typically produce burst suppression. *Propofol* - **Propofol** generally produces a **decrease in EEG activity**, progressing to **burst suppression** and then an isoelectric EEG at higher doses, reflecting its profound cerebral depressant effects. - It significantly **reduces cerebral metabolic rate (CMR)** and **intracranial pressure (ICP)**, making it useful in neurosurgery. *Thiopental* - **Thiopental**, a barbiturate, profoundly **decreases EEG activity**, leading to **burst suppression** and an isoelectric EEG at increasing doses. - It significantly **reduces cerebral metabolic rate of oxygen consumption (CMRO2)**, cerebral blood flow (CBF), and intracranial pressure (ICP), providing **neuroprotection**. *Ketamine* - **Ketamine** is unique in that it causes a dissociation between the limbic system and thalamocortical system, leading to a **dissociative anesthetic state** characterized by **increased EEG activity** and disorganized patterns. - It **increases cerebral metabolic rate (CMR)**, cerebral blood flow (CBF), and intracranial pressure (ICP), which can be a concern in patients with pre-existing neurological conditions.

Question 8: A hyperventilating patient has the following ABG values: pH=7.53, pCO2=20 mmHg, HCO3= 26 mEq/L. What is the most likely diagnosis?

A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory alkalosis (Correct Answer)
D. Respiratory acidosis

Explanation: ***Respiratory alkalosis*** - The pH of 7.53 indicates **alkalemia**, and the low pCO2 (20 mmHg) is the primary driver, signifying **respiratory alkalosis** - A hyperventilating patient exhales more CO2, leading to a decrease in its partial pressure in the blood and a subsequent rise in pH - The HCO3 is within normal range (26 mEq/L), indicating **uncompensated respiratory alkalosis** *Metabolic alkalosis* - This would be characterized by a high pH and an elevated **HCO3**, but the HCO3 is within the normal range (26 mEq/L) - While it causes alkalemia, the primary disturbance here is respiratory, not metabolic *Metabolic acidosis* - This would present with a **low pH** and a low **HCO3**, which is contrary to the given ABG values - The patient's pH is elevated, indicating an alkalotic state, not acidotic *Respiratory acidosis* - This would be defined by a **low pH** and an elevated **pCO2**, which is the exact opposite of the provided ABG results - The patient's high pH and low pCO2 rule out respiratory acidosis

Question 9: All of the following are true about Status marmoratus:

A. Associated with asphyxia
B. Present in basal ganglia
C. Have a marbled appearance
D. All of the options (Correct Answer)

Explanation: ***All of the options*** - This is the correct answer because **all three statements accurately describe Status marmoratus**. - Status marmoratus is a well-defined neuropathological finding with characteristic features that include association with asphyxia, localization to basal ganglia, and marbled gross appearance [1]. **Key Features of Status Marmoratus:** *Associated with asphyxia* - Status marmoratus is a classic sequela of **perinatal hypoxic-ischemic injury** (birth asphyxia) [1]. - Results from severe and prolonged oxygen deprivation during the perinatal period [1]. - The hypoxic injury leads to selective neuronal loss in vulnerable brain regions. *Present in basal ganglia* - The characteristic lesions are located in the **basal ganglia** (especially putamen and caudate) and **thalamus** [2]. - These deep gray matter structures are particularly vulnerable to hypoxic-ischemic injury [2]. - This distribution explains the extrapyramidal movement disorders (choreoathetosis, dystonia) seen clinically [1]. *Have a marbled appearance* - The term "marmoratus" means **marbled** in Latin, describing the gross pathological appearance. - The marbling results from **abnormal myelination** in damaged areas mixed with **gliosis** and loss of neurons. - On sectioning, there is a distinctive pattern of white (myelinated fibers) streaking through gray matter, creating a marble-like appearance. - Microscopically shows neuronal loss, gliosis, and status dysmyelinatus. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1260-1261. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1266-1268.

Question 10: Which of the following is a key clinical feature of hypoxic ischemic encephalopathy?

A. Lower limbs affected more than upper limbs
B. Proximal muscle weakness is more pronounced than distal muscle weakness
C. Seizures (Correct Answer)
D. Trunk muscle weakness

Explanation: ***Seizures*** - **Seizures** are a common and significant clinical feature of **hypoxic ischemic encephalopathy (HIE)**, reflecting the acute neuronal injury and dysfunction caused by oxygen deprivation. - They can occur early in the course of HIE and may manifest in various forms, including tonic-clonic, myoclonic, or subtle seizures. [1] *Lower limbs affected more than upper limbs* - This pattern of motor dysfunction is more characteristic of conditions like **cerebral palsy** with **spastic diplegia**, which can be an outcome of HIE but is not a primary acute clinical feature of HIE itself. - While HIE can cause motor deficits, the immediate presentation does not typically involve disproportionate lower limb involvement without other severe neurological signs. *Proximal muscle weakness is more pronounced than distal muscle weakness* - While muscle weakness can occur in HIE due to diffuse brain injury, a specific pattern of **proximal over distal weakness** is not a hallmark clinical feature of the acute phase. - This pattern may be seen in certain muscular dystrophies or myopathies, which are distinct from HIE. *Trunk muscle weakness* - **Trunk muscle weakness** can be a part of generalized hypotonia or motor dysfunction in severe HIE, but it is not as specific or as immediately indicative of HIE as the presence of acute seizures. - While important for overall motor function, it is not considered a primary or defining clinical feature for the initial diagnosis of HIE.

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free