FETAL MONITORING

Maternal health is the most important determinant of fetal well-being, affecting its health in many ways (Table 12.3). The term ‘fetal monitoring' refers to clinical, radiological, physiological and biochemical evaluation of fetus in utero, though last two steps are necessary only in selected cases.

I. Assessment of gestational duration by:

• Last menstrual period (LMP): Expected date of delivery (EDD) may be calculated by advancing LMP date with 9 months and 7 days.

Uterine fundal height (UFH) is a reliable indicator of gestational length, except in last trimester. UFH is ~20 cm at 20 weeks and 28 cm at 28 weeks Disproportionately more UFH indicates multiple

pregnancy, polyhydramnios, and fibroids.

• Fetal events, e.g. appearance of heart sounds (16-20 weeks) and quickening (18-20 weeks) are not very reliable indicators of gestational length.

Swallowing is a voluntary as well as reflex activity, initiated by the presence of food or saliva in oral cavity and requires close coordination between—(a) closure of nasopharynx by soft palate to prevent nasal regurgitation, (b) closure of glottis to prevent aspiration and (c) relaxation of upper esopharyngeal sphincter to transfer food bolus into esophagus. Further esophageal passage is facilitated by peristaltic waves, culminating into relaxation of lower esophageal sphincter and transfer of food into stomach.

Dysphagia, i.e. difficulty during deglutition indicates either obstruction in food passage (Mechanical dysphagia) or neuromuscular incoordination in swallowing mecha­nisms (Transfer dysphagia).

Etiology: Foreign body ingestion is the commonest cause of acute dysphagia in childhood, while chronic dysphagia may be due to impacted foreign bodies or bulbar/pseudobulbar palsy (Table 14.2).

Diagnostic evaluation in dysphagia includes:

Detailed history, specially for foreign body ingestion, and relationship of dysphagia with type of foods.

• Throat examination to exclude local pathology, and detailed neurological evaluation for neuromuscular disorders.

• Relevant investigations, e.g. (a) X-rays for foreign body, (b) barium swallow for strictures, foreign

Acyanotic CHDs may be broadly divided into two cate­gories - those with volume overload, i.e. Lt gt; Rt shunts, and those with pressure overload, i.e. obstructive lesions.

Acyanotic CHDs with volume overload are characterized by Lt gt; Rt shunt with re-circulation of oxygenated blood back to the lungs. Magnitude of shunt depends on the size of defect and pressure gradient between pulmonary and systemic circuits. As these factors are dynamic, pathophysiology and clinical picture may change with age, as follows:

Since pulmonary vascular resistance is high at birth due to poorly expanded lungs, Lt gt; Rt shunt is

minimum in newborns with no murmurs. Murmurs generally appear after a few days, as pulmonary arterial pressure drops below the systemic pressure.

Spastic paraplegia is usually seen below the level of spinal cord lesions, commonest being spinal tuberculosis (Pott's spine), spinal injuries and neural tube defects.

• Flaccid paraplegia usually indicates anterior horn cell disease, e.g. poliomyelitis, acute transverse myelitis or neuropathies, e.g. Guillain-Barre Syndrome (GBS) and traumatic neuritis.

Diagnostic approach in paraplegia aims to—(a) localize the site of lesion, and (b) identify probable etiology. Important steps in evaluation include:

Step I. Whether paraplegia is spastic or flaccid?

Spastic paraplegia is characterized by UMN signs, e.g. spasticity, hyperreflexia and extensor planter response, usually due to thoracic or lumbar cord lesions. Cervical cord lesions present with quadriparesis.

Flaccid paraplegia with LMN signs, i.e. hypotonia, hyporeflexia and flexor planter response, is usually seen in neuromuscular disorders or in spinal shock (first few days after acute spinal injury, before signs of UMN lesions appear).

Acute, symmetrical and ascending muscle weakness indicates GBS, while muscle weakness is typically acute and asymmetrical.

Atrophy or pseudohypertrophy of muscles indicates neuropathy or myopathy, respectively. Muscle weakness

Growth hormone (GH) deficiency is a leading cause of short stature in childhood.

GH secretion is regulated by two important hypo­thalamic hormones - GHRH (releasing hormone, Ghrelin) and GHIH (inhibiting hormone, somatostatin). Alternate secretion of these two regulators is responsible for characteristic pulsatile release and diurnal rhythm in GH secretion, being highest during night. GH secretion is stimulated by sleep, exercise and hypoglycemia and inhibited by steroids, which also oppose its action on target tissues.

GH acts on various tissues by increasing the synthesis of an insulin-like growth factor (IGF₁) in liver and growth plates. Another mediator, IGF₂ has been identified as an important mitogen in bone cells with uncertain role. Etiology: While GH deficiency is usually a part of MPHD in acquired lesions, isolated deficiency (IGHD) is more common, which is usually genetic and may be quantitative or qualitative. Common causes of IGHD include:

• Genetic or quantitative IGHD (AR, AD or X-linked)

• Biologically-inactive GH (qualitative defect)

• GH-receptor insensitivity (Laron syndrome)

Hyperpituitarism in children is very rare and caused by hormone-secreting adenomas, commonest being prolac­tinoma, followed by corticotropinoma, somatotropinoma and rarely thyrotropinoma or gonadotropinoma.

Clinically, most cases present either with only tall stature or broad-spectrum syndromes, e.g. acromegaly or gigantism. Gigantism is caused by overproduction of GH before the closure of epiphyses in younger children (less common), while acromegaly is a feature of late disease after closure of epiphysis. Consequently, gigantism is mainly characterized by tall stature while following features are more common in acromegaly:

• Tall stature, often with kyphosis.

• Typical facial features with macrocrania, broad nose, long tongue and prognathia with separation of teeth.

• Disproportionately long and thick fingers/toes.

SECRETION (SIADH)____________________________________

SIADH is a common and important cause of dys­electrolytemia in critical care units, denoting quot;dispro­portionately high plasma ADH levels as compared to plasma osmolality, leading to excessive urinary concen­tration, fluid retention and dilutional hyponatremiaquot;.

Etiologically SIADH is either due to increased ADH secretion from hypothalalmus or secretion of other ADH-like vasopeptides from neoplastic tissues. SIADH is commonly seen in:

• Acute CNS disorders, e.g. intracranial infections, head injury, subarachnoid hemorrhage, etc.

• Critically sick children due to any cause, e.g. pneu­monia, post-surgery, invasive ventilation, etc.

• Neoplastic states, e.g. leukemia, lung and pancreatic tumors, etc.

Clinical manifestations are often dominated by features of causative disease, along with:

• Signs of water intoxication, e.g. vomiting/nausea and irritability,

• Signs of hyponatremia, e.g. seizures, stupor or coma. Diagnosis of SIADH should be suspected in any criti­cally sick baby with: (a) hyponatremia, and (b) high urine osmolality despite low serum osmolality.

Management includes: (a) Restricted fluid intake to only 2/3^rd of maintenance requirements, (b) correction of hyponatremia and other electrolyte abnormalities, and (c) treatment of primary cause.

Demeclocycline, which blocks the ADH action on collecting tubules, may be used in selected cases. Vasopressin receptor antagonists, i.e. Conivaptan or Tolvaptan also increase free water clearance.

Signs:

No sign of pneumonia/severe pneumonia

Treatment:

• Inhaled/ oral salbutamol for 5 days, if wheezing

• Safe home remedies¹ in children gt; 6 months

• Follow-up after 5 days or SOS

• Referral, if cough persists for gt; 30 days

Signs:

No signs of bacterial infection/very severe disease

Treatment:

• Advise home care

Accordingly, all babies are classified in following three categories—(a) severe jaundice, (b) jaundice, (c) no jaundice (Table 29.8).

Step III. Assessment for diarrhea: All sick young infants should be assessed for the presence and severity of diarrhea, i.e. increased frequency and/or liquidity of stools from the usual pattern. Note that even normal stools in breast-fed infants are generally more frequent and liquid and should not be construed as diarrhea.

All sick young infants with diarrhea must be assessed for—(a) dehydration, and (b) blood in stools. Presence of dehydration is assessed by—(a) general condition, spontaneous movements, sluggish movements or movements only on stimulation, no movements on stimulation or irritability/restlessness, (b) sunken eye balls, and (c) loss of skin turgor.

Accordingly, these cases are classified in three categories—(a) severe dehydration, (b) some dehy­dration, (c) no dehydration, (Table 29.9). Presence of blood in stools needs referral for evaluation.