Abdominal Pain
Abdominal pain is a common complaint in children. The extensive differential diagnosis (Table 9.1) necessitates a systematic approach to make an accurate diagnosis.
Clinical Presentation
Visceral pain receptors in the abdominal serosa responding to mechanical and chemical stimuli, such as stretching, tension, and ischemia, send signals to the spinal cord resulting in poorly localized, ill-defined pain. Upper gastrointestinal (GI) pathology manifests as epigastric discomfort; distal small bowel and proximal colonic diseases are perceived as periumbilical pain; and distal colonic pain is referred to the lower abdomen. Conversely, stimulation of the somatoparietal pain receptors in the parietal peritoneum causes localized pain on the same side and at the same dermatomal level as the source of the pain. Parietal pain is usually sharp, well-defined, and aggravated by movement or cough. Referred pain is similar to parietal pain, but occurs at a site distant to, but supplied by the same dermatome as, the involved organ. Non-GI causes, such as genitourinary infections and pneumonia, can also manifest as abdominal pain and must be considered on the differential for a patient with abdominal pain.
Diagnosis
Obtain a thorough history and assess for worrisome symptoms, such as weight loss, unexplained fevers, dysphagia, bilious emesis or hematemesis, chronic unexplained diarrhea, hematochezia or melena, poor growth or delayed puberty. Ask about the duration, quality, intensity, location, and radiation of the pain. Also note the response to defecation, urination, meals, and change in position. Determine if there is upper or lower GI bleeding, fever, vomiting, diarrhea, night or early morning awakening, weight loss, or growth failure. Inquire about respiratory, cardiovascular or urinary symptoms, stooling habits, menstrual cycle, testicular pain, sexual activity, and the possibility of pregnancy. Ask about past illnesses, medication, travel, trauma, family and social history, and exposure to animals or sick contacts.
Although a definitive diagnosis cannot always be made immediately, a primary goal is the early recognition of surgically correctable emergencies and potentially unstable conditions.
Start with assessing vital signs and then begin the examination with the non-threatening and painless components, leaving the abdominal and rectal examinations for the end. Quickly assess the patient’s hydration status and cardiovascular/respiratory stability. Try to elicit and localize abdominal tenderness, as well as rebound tenderness or masses. A pelvic exam is necessary for all sexually active or postmenarchal females with lower abdominal pain. Perform a testicular examination for males.
In an infant, suspect an intra-abdominal surgical emergency such as malrotation with midgut volvulus or intussusception whenever there is a history of bilious or projectile vomiting and/or bleeding. The signs may be preceded or accompanied by irritability, poor feeding, and lethargy. Suspect a surgical condition if the physical examination reveals abdominal distension, a scaphoid abdomen, localized abdominal tenderness or guarding, a mass, high-pitched or absent bowel sounds, or if the patient is ill-appearing. A patient with peritoneal irritation will often remain motionless, whereas a patient with visceral pain is usually changing positions and writhing in discomfort.
ED Management
If the etiology of the abdominal pain is unclear and the patient has persistent, severe symptoms, obtain a CBC, electrolytes, liver function panel, amylase, lipase, inflammatory markers, urinalysis, and stool guaiac. Obtain a pregnancy test for any postmenarchal female. If the patient has been vomiting or is dehydrated, give a 20 mL/kg NS intravenous (IV) bolus, followed by maintenance fluids either IV or oral, if tolerated. Give one oral dose of ondansetron (8–15 kg: 2 mg; 6–30 kg: 4 mg; >30 kg: 8 mg). Obtain an abdominal ultrasound if there is suspicion for appendicitis, hepatobiliary disease, pancreatitis, renal disease, or pregnancy based on laboratory values.
See the specific sections for the work-up for other etiologies, such as appendicitis (pp. 241–244), cholelithiasis (pp. 260–263), hepatitis (pp. 268–272), intussusception (pp. 273–274), Meckel’s diverticulum (pp. 282–283), ovarian cyst (pp. 323–325), and pancreatitis (pp. 238–241). If the work-up is inconclusive and the patient continues with severe or focal pain, admit for serial abdominal examinations. Further ED evaluation by pediatric surgery is warranted for focal pain or signs of peritonitis. Consult pediatric gastroenterology if surgical emergencies have been ruled out and the etiology is still unclear.
Follow-up
Indications for Admission
Dehydration or inability to take fluids
Persistent, severe abdominal pain
Bibliography
Acute Pancreatitis
Acute pancreatitis is a serious cause of abdominal pain in children. While pancreatitis is associated with many conditions, up to 30% of cases are idiopathic (Table 9.2). Premature activation of digestive enzymes, particularly trypsinogen, causes injury of the pancreatic acinar cells. This can precipitate a systemic inflammatory response, oxidative stress, edema, and, in severe cases, necrosis of the gland with associated multiorgan failure.
| Anatomic | Annular pancreas, pancreas divisum, sphincter of Oddi dysfunction |
| Biliary | Biliary sludge, choledochal cyst, cholelithiasis |
| Genetic | Hereditary pancreatitis, trypsinogen gene mutation, |
| Infections | Coxsackie B, echovirus, Epstein–Barr virus, hepatitis (A and B), HIV, |
| influenza A, leptospirosis mumps, Mycoplasma, Salmonella | |
| Mechanical | Blunt abdominal trauma (including child abuse), S/P ERCP |
| Medications | Alcohol, anticoagulants, azathioprine, borate, chlorthiazide, |
| corticosteroids, cytarabine, ethanol, indomethacin, isoniazid, L-asparaginase, mercaptopurine, mesalamine, salicylic acid, tetracycline, valproic acid | |
| Metabolic | Alpha-1 antitrypsin deficiency, diabetes, hypercalcemia, |
| hypertriglyceridemia | |
| Nutritional | Malnutrition, vitamin A and D deficiency |
| Systemic disease | Anorexia nervosa, cystic fibrosis, inflammatory bowel disease, juvenile |
| idiopathic arthritis, polyarteritis nodosa, Reye syndrome, systemic lupus | |
| erythematosus | |
| Other | Familial, idiopathic |
Clinical Presentation
The classic symptoms of acute pancreatitis are abdominal pain, nausea, vomiting, and anorexia. The pain is typically located in the epigastrium, right upper quadrant, or periumbilical area, with radiation to the back or lower chest. Both the pain and vomiting are worsened by eating. Younger patients may present with subtle symptoms of vomiting, lethargy, and irritability. Other associated symptoms include fever, jaundice, diarrhea, or clay-colored stools.
On physical examination the patient is often tachycardic, and sometimes hypotensive early in the disease. There may be tenderness in the upper abdomen, and the patient may refuse to lie supine. Guarding, rebound tenderness, abdominal distension, and decreased bowel sounds can mimic an acute surgical abdomen. With severe hemorrhagic pancreatitis, serosanguinous fluid may track through fascial planes resulting in blue discoloration of the flanks (Grey-Turner sign) or the umbilicus (Cullen sign). Signs of ascites (shifting dullness, fluid wave) or pleural effusion (decreased bowel sounds, friction rub, dullness to percussion) may be present if the disease is advanced. Patients with severe acute pancreatitis will present in shock with signs and symptoms of multiorgan failure, including shortness of breath, oliguria, hemorrhage, or change in mental status.
Diagnosis
The diagnosis of acute pancreatitis is confirmed when the patient has two or three of the following findings:
clinical symptoms consistent with acute pancreatitis including abdominal pain, nausea, vomiting, or back pain;
serum amylase or lipase ≥3 times the upper limit of normal;
radiographic (CT or ultrasound) evidence of acute pancreatitis.
Lipase is more sensitive and specific than amylase in acute pancreatitis. A normal amylase does not rule-out acute pancreatitis, while an elevated amylase level can occur in a variety of other conditions (Table 9.3). In addition, the degree of elevation does not correlate with disease severity.
| Biliary |
| Bile duct obstruction |
| Cholecystitis |
| Intestinal |
| Appendicitis |
| Intestinal obstruction |
| Perforated peptic ulcer |
| Pancreatic |
| Acute or chronic pancreatitis |
| Pancreatic duct obstruction |
| Pancreatic tumor |
| Salivary |
| Parotitis |
| Salivary duct obstruction |
| Trauma |
| Miscellaneous |
| Burns |
| Diabetic ketoacidosis |
| Macroamylasemia |
| Pregnancy (ruptured ectopic) |
| Renal insufficiency |
In suspected acute pancreatitis, obtain a CBC, electrolytes including glucose, calcium, magnesium, liver function tests (bilirubin direct and total, gamma-glutamyl transpeptidase [GGT], alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase), and a triglyceride level. Other laboratory abnormalities that occur with severe pancreatitis include hypocalcemia, hypomagnesemia, hyperglycemia, and hemoconcentration. If there is associated cholelithiasis, there may be elevations of direct bilirubin, GGT, and alkaline phosphatase.
Radiologic confirmation requires either abdominal ultrasound or a CT scan. Ultrasound can document the presence of a pancreatic pseudocyst, dilated ducts, cholelithiasis, abscesses, or ascites. Abdominal CT scan is helpful in suspected traumatic pancreatitis and can provide better visualization of masses, necrosis, and hemorrhage. Imaging can also detect associated injury to the liver, spleen, and duodenum. In patients with respiratory signs or symptoms, obtain a chest x-ray to assess the disease severity and to rule-out pleural effusions, ARDS, or pneumonia.
ED Management
The management of pancreatitis is supportive. Keep the patient NPO in an effort to “rest” the pancreas and prevent stimulation of pancreatic exocrine secretions. Start an IV and aggressively treat signs of hypovolemia with 20 mL/kg boluses of an isotonic solution (LR or NS). Closely monitor the patient’s hydration status, as there may be ongoing leakage of fluid into the interstitial space. Provide sufficient fluid to maintain adequate circulation. Give an H2 blocker IV to help prevent stress ulceration (ranitidine 8 mg/kg/day div q 8h, 50 mg/dose maximum; famotidine 0.6–0.8 mg/kg/day div q 12h, 40 mg/dose maximum). Reserve antibiotics for clinical signs of sepsis, necrotic pancreatitis, cholangitis, or multiorgan system failure.
Manage pain with morphine 0.05 mg/kg/dose IV or subcutaneously every 2–4 hours. Alternatives include fentanyl (0.5–1 mcg/kg/dose q 1–2h) or meperidine (0.5 mg/kg/dose q 2–4h), but with repeated doses there is the risk of the accumulation of neurotoxic metabolites, which may cause seizures. If the patient requires multiple doses of narcotic analgesia, use a fentanyl or morphine drip via a patient-controlled analgesia (PCA) pump.
Admission to an ICU is indicated for severe complications such as shock, impending renal failure, hypoxia, or significant metabolic derangements. In addition, supplemental calcium (see pp. 191–193), magnesium, and insulin may be needed.
Indications for Admission
Acute pancreatitis
Bibliography
Appendicitis
Appendicitis is the most common childhood illness requiring emergency surgery, with a peak incidence in the second decade of life. It begins with obstruction of the appendiceal lumen, often secondary to an appendicolith or lymphoid hyperplasia, leading to distention. If not recognized in time, necrosis of the wall of the appendix occurs, followed by perforation and subsequent peritonitis. Early diagnosis is of paramount importance.
Clinical Presentation
In uncomplicated appendicitis (prior to rupture), there is a short history (usually <36 hours) of abdominal pain, anorexia, nausea, and vomiting. Early in the course colicky or persistent periumbilical pain is typical. The pain then shifts to the right lower quadrant where it is constant and severe. Low-grade fever (<38.3 °C;101 °F) is common, and a change in stool pattern occurs in about 15% of patients. Other symptoms may include dysuria or labial, testicular, or penile pain. Maintain a high index of suspicion, as many patients do not have a “classical” presentation.
On physical examination tenderness is greatest over McBurney’s point (one-third of the distance along a line from the anterior superior iliac spine to the umbilicus). There may be positive psoas (pain on passive hip hyperextension consistent with retrocecal appendix) and/or obturator (pain on passive internal rotation of the thigh consistent with pelvic appendix) signs. In the case of a retrocecal appendix, the maximum tenderness and rigidity may remain in the periumbilical area or in the right flank. While palpating the left lower quadrant, discomfort may be elicited in the right lower quadrant (Rovsing’s sign). Rigidity of the abdominal wall, diffuse tenderness, and involuntary guarding are suggestive of perforation.
Perforation occurs in 20–40% of patients and, although the incidence varies with age, it is seen most frequently in children under four years old. Other signs of rupture include pain for more than 36 hours, frequent vomiting, dyspnea secondary to elevation of the diaphragm, lethargy in the young child, and a temperature >38.5 °C (101.3 °F).
Diagnosis
A careful history and physical examination are the keys to diagnosing appendicitis. Defer the abdominal and rectal examinations for last. Gently palpate the abdomen beginning away from the right lower quadrant. If the patient’s responses do not seem accurate, palpate the abdomen with the membrane of the stethoscope, as the child will believe that auscultation, and not palpation is being performed. Since appendicitis is a progressive disease, increasing abdominal pain, tenderness, and rigidity on serial physical examinations are highly suggestive of the diagnosis.
Try to elicit rebound tenderness which occurs with inflammation of the peritoneum. To do this in a younger child, shake or percuss the abdomen, tap firmly on the feet, or ask the patient to cough, jump down from the table, or hop. In an older patient, depress the abdomen for 5–10 seconds, then withdraw your hand suddenly. Rebound tenderness is confirmed by finding pain on release, rather than during direct pressure.
The differential diagnosis of appendicitis is extensive, as shown in Table 9.4. If the diagnosis remains unclear, perform a rectal examination. Right-sided tenderness is consistent with appendicitis, whereas hard stool in the vault is suggestive of constipation, which can mimic appendicitis, although some constipated patients will be fidgety or “dancing,” and will not keep still. Also perform a pelvic exam and obtain urine for a pregnancy test in sexually active females and perform a genital exam, including the cremasteric reflex, to rule-out testicular torsion in a male.
| Diagnosis | Differentiating features |
|---|---|
| Bacterial enteritis | Guaiac positive stools and fecal leukocytosis |
| Bowel obstruction | Crampy, periumbilical pain |
| Abdominal distention | |
| Cholecystitis | RUQ pain with positive Murphy’s sign |
| Cholelithiasis | RUQ colicky pain |
| Constipation | Pain is nonmigratory and is relieved upon defecation |
| Stool palpated in descending colon and ampulla | |
| Diabetic ketoacidosis | Polyuria, polydypsia, polyphagia |
| Kussmaul respirations | |
| Intussusception | Pain and vomiting alternating with periods of lethargy |
| Afebrile | |
| 80% of patients are <2 years old | |
| Ectopic pregnancy | Positive pregnancy test |
| Vaginal bleeding | |
| Functional abdominal pain | Recurrent attacks of abdominal pain |
| No vomiting, diarrhea, fever, or weight loss | |
| Henoch–Schönlein purpura | Pain may precede the rash |
| Hepatitis | RUQ tenderness and jaundice (variable) |
| Inflammatory bowel disease | Recurrent episodes of pain |
| Bloody diarrhea and abdominal distention | |
| Intrauterine pregnancy | Positive pregnancy test |
| Mesenteric adenitis | Diagnosis of exclusion |
| Pancreatitis | Epigastric pain that may radiate to the back |
| Pelvic inflammatory disease | Pain in lower abdomen |
| Vaginal discharge or bleeding | |
| Pneumonia | Tachypnea may be present |
| Testicular torsion | Tender, swollen, erythematous hemiscrotum |
| Abnormal cremasteric reflex | |
| Urinary tract infection | Frequency, urgency, dysuria, and flank pain |
| Pyuria | |
| Urolithiasis | Colicky pain with gross or microscopic hematuria |
| Viral gastroenteritis | Vomiting prior to, or simultaneously with, abdominal pain |
| Abdominal pain relieved by vomiting or a bowel movement | |
| Diarrhea may be prominent |
ED Management
When the diagnosis is evident from the history and physical examination, make the patient NPO, start maintenance IV hydration with D5 ½ NS, obtain a CBC, electrolytes, urinalysis, type and screen, and consult a surgeon. If there is evidence of intravascular depletion (orthostatic vital sign changes, delayed capillary refill, hypotension), give the patient a bolus of 20 mL/kg of NS or lactated Ringer’s.
In general, abdominal x-rays are not necessary. However, a KUB may confirm constipation, or reveal an appendicolith (10% of cases), soft tissue mass, or focal ileus in the right lower quadrant consistent with the diagnosis of appendicitis.
Perform an ultrasound to evaluate the appendix, although the findings may be limited in an obese patient. A diagnostic examination may show a fluid-filled, non-compressible, distended, tubular mass >6 mm. Perform a CT scan with IV contrast only if the diagnosis remains unclear or it is likely that the patient has an abscess. CT findings in acute appendicitis include: appendicular diameter of >6 mm; appendicolith; pericecal fat stranding; thickening of adjacent bowel walls; free peritoneal fluid; lymphadenopathy; and the presence of a phlegmon. However, MRI is preferred over CT scan if available, given its lack of radiation.
A mildly elevated WBC and CRP is supportive of a diagnosis of appendicitis and a WBC >15,000/mm3 suggests rupture or another bacterial process (pneumonia, bacterial gastroenteritis). Do not delay surgical evaluation if these values are normal in a patient with a clinical picture that is suggestive of appendicitis. Obtain a chest x-ray if there is tachypnea, rales, other pulmonary signs, or an elevated WBC in a child with a negative abdominal CT scan.
Serum electrolytes may be helpful in patients with abdominal pain and dehydration. A low serum sodium (<130 mEq/L) may reflect third-spacing of fluids from the ileus associated with a ruptured appendicitis. A urinalysis is necessary to rule-out diabetic ketoacidosis (glycosuria and ketonuria) or a urinary tract infection (bacteriuria and pyuria). Although there can be WBCs in the urine with an appendicitis, bacteriuria is typically absent.
Once the diagnosis of appendicitis has been made, and agreed upon by the surgical team, start antibiotic therapy. If a non-perforated appendicitis is suspected, give cefoxitin (40 mg/kg; 2 g maximum) or cefotetan (30 mg/kg/day div q 12h; 6g/day maximum) IV, while awaiting appendectomy. If a perforated appendicitis is suspected, give broader antibiotic coverage to prevent or minimize intraperitoneal abscess formation. Use monotherapy with piperacillin-tazobactam (350 mg/kg/day divided q 6h; 3g/dose maximum; use 175 mg/kg/day for infants <6 months) IV.
The appropriate use of analgesia does not impair diagnostic accuracy. Give morphine subcutaneously or IV (0.1 mg/kg; 5 mg maximum for the initial dose; titrate subsequent doses based upon clinical effect). Do not use nonsteroidal medications such as ketorolac if there is a possibility of surgical intervention, as this class of drugs inhibits platelet function and can cause excessive bleeding.
When appendicitis cannot be excluded, admit the patient for IV hydration and observation and keep them NPO.
Follow-up
Indications for Admission
Suspected or confirmed appendicitis
Bibliography
Assessment and Management of Dehydration
The most common causes of dehydration in children are vomiting (pp. 289–293) and diarrhea (pp. 255–260).
Clinical Presentation and Diagnosis
Dehydration is classified by the percentage of total body water lost: mild (<5%), moderate (5–10%), and severe (>10%). A variety of signs and symptoms and ancillary data help to distinguish the degree of dehydration (Table 9.5). The most objective measure is an acute change in weight from the premorbid state, which reflects fluid loss.
| Signs/symptoms | Mild (<5%) | Moderate (5–10%) | Severe (>10%) |
|---|---|---|---|
| Abnormal skin turgor | – | +/– | + |
| Altered mental status | – | +/– | + |
| Capillary refill time >2 s | – | +/– | + |
| Decreased urine output | +/– | + | + |
| Depressed fontanelle | – | + | + |
| Dry mucous membranes | + | + | + |
| Hyperpnea | – | – | + |
| Hypotension | – | – | + |
| Orthostatic vital sign changes | – | +/– | + |
| Serum acidosis | – | +/– | + |
| Sunken eyeballs | – | + | + |
| Tachycardia | +/– | + | + |
| Urine specific gravity | Normal/high | Normal/high | High |
| Weak peripheral pulses | – | – | + |
ED Management
The management priorities are stabilization of the patient’s vital signs, replenishment of the intravascular volume, and correction of electrolyte abnormalities.
No Dehydration
If the patient has diarrhea but is not dehydrated and appears well, give clear fluids to maintain hydration, as well as an age-appropriate diet as tolerated. Allow a breastfed infant to continue to nurse. If the patient also is vomiting, give small amounts of clear fluids (see Mild and Moderate Dehydration below). Confirm that all infants and children can tolerate oral fluids prior to discharge.
Mild and Moderate Dehydration
A patient with mild or moderate dehydration can be orally rehydrated, if willing and able to tolerate fluids.
Vomiting
If the patient has been vomiting, wait 30–60 minutes after the last episode to initiate oral fluids. Use an oral rehydration solution (ORS) containing 60–90 mEq/L of sodium and 20–25 g/L of glucose. Give an infant (<1 year of age) small (5–10 mL) aliquots and an older child a larger amount (10–20 mL) of fluid every 5–15 minutes, over the next hour, followed by reassessment of the hydration status. If a patient with gastroenteritis is unable to tolerate the fluid, give one dose of ondansetron (see p. 292). Once the patient looks well and has stopped vomiting, discharge him or her with written instructions on how to advance the diet by increasing the amount of ORS over 8–12 hours.
Diarrhea
Start rehydration with an ORS. Give a total volume of 40–50 mL/kg in small aliquots (15–30 mL) over a 3–4 hour period, while doing hourly reassessments of hydration status. Failure of oral rehydration (inability to take adequate volume orally, excessive ongoing losses) is an indication for IV rehydration therapy. Once the initial rehydration is tolerated, resume giving milk (breast or formula) to an infant. If an infant has large, watery stools, supplement the milk with feedings of an ORS. For older infants and toddlers already taking solid foods, recommend an ORS, with a low-fat carbohydrate diet. Anti-diarrheal compounds and anti-motility agents have no role in the management of acute diarrhea.
Severe Dehydration
IV fluid restoration is necessary for severe dehydration, shock, altered mental status or if the patient is unable to take fluids orally.
Initial Intravascular Restoration
Initiate fluid resuscitation with a 20 mL/kg bolus of normal saline or lactated Ringer’s solution over 20–30 minutes. Obtain blood for electrolytes, BUN, creatinine, lactate and glucose. Also obtain a urinalysis, and if the urine contains large ketones or if the child is hypoglycemic, add 2 mL/kg of D25 (0.5 g/kg of glucose) to the bolus solution. After the first bolus, reevaluate the patient using parameters outlined in Table 9.5. If there is a poor response to the initial bolus, repeat the infusion. Patients with renal or cardiac disease are at risk for developing congestive heart failure and patients with sickle cell disease are at risk for acute chest syndrome. Therefore, carefully and thoroughly assess their fluid status. If there is a poor response to three IV boluses, consider other associated organ disease, such as sepsis, myocarditis, and neurogenic shock, or the need for central venous monitoring before giving additional boluses. Following the restoration of adequate intravascular volume, assess the need for replacement of fluid and electrolyte deficits.
Calculate maintenance fluids using the Holiday–Segar method:
100 mL/kg/day for the first 10 kg (1000 mL/day) or 4 mL/kg/h for the first 10 kg;
50 mL/kg/day for the next 10 kg (500 mL/day) or 2 mL/kg/h for the next 10 kg;
20 mL/kg/day for each additional kg or 1 mL/kg/h for each additional kilogram.
Replacement of Fluid and Electrolyte Deficits
Isotonic Dehydration
In isotonic dehydration the serum sodium is between 130 mEq/L and 150 mEq/L. Estimate the percentage of dehydration either by physical signs and symptoms or, more accurately, if a recent premorbid weight is known. Multiply the percentage of dehydration by the weight of the child to calculate the fluid deficit (e.g., 10% dehydration × 20 kg child = a deficit of 2 L). Administer maintenance fluid requirements plus half of the deficit over the first 8 hours and the second half over the following 16 hours. Sodium requirements are 2–4 mEq/kg/day. In general, either D5 ½ NS (≥2 years of age) or D5 ⅓ NS (<2 years of age) is an adequate solution. Potassium requirements are 2–3 mEq/kg/day. After the patient has voided, add potassium chloride (20–40 mEq/L) to the IV bag.
Hypotonic Dehydration
Hypotonic dehydration occurs when salt losses exceed water losses or when water intake exceeds required salt intake. Hyponatremia is defined as serum sodium <130mEq/L. Use the following formula to calculate the sodium deficit to be added to the replacement fluids (see Hyponatremia, pp. 197–200):
Give the sodium replacement over four hours, but do not exceed a rate of correction of more than 0.5–1 mEq/h. An excessively rapid correction of the serum sodium may be associated with central pontine myelinolysis.
Symptomatic hyponatremia (seizures) requires a more rapid correction with hypertonic 3% saline. Three percent saline contains 513 mEq/L of Na, so that every 2 mL contains 1 mEq Na. One mL/kg of 3% NaCl will increase the plasma sodium by approximately 1 mEq/L. The initial goal is to raise the serum sodium by 5 mEq, which is usually sufficient to terminate the seizures; calculate the amount of 3% NaCl (mL) required as follows:
Multiply the results by 2 to determine the volume in milliliters.
Hypertonic Dehydration
Hypernatremia is defined as a serum sodium >150 mEq/L. It occurs when solute-free water losses exceed salt losses or in the context of excessive salt intake. The degree of dehydration is more difficult to determine in these patients because the extracellular fluid space is preserved. The skin may have normal turgor but feel doughy. Calculate the free water deficit as follows:
(Use 3 mL/kg for serum sodium >170 mEq/L.)
Because of the potential for neurologic complications, correct the serum sodium and free water deficit slowly over 48 hours, with a daily sodium decrease of 10–15 mEq/L (approximately 0.5 mEq/h). In general, D5 ½ NS is an appropriate solution. Add 40 mEq/L of potassium acetate after the patient voids (see Hypernatremia, pp. 188–191).
Calculation Examples
10 kg (Premorbid Weight) Child With 10% Isotonic Dehydration (Sodium = 140mEq/L)
Give half of deficit in the first 8 hours and the remaining half in the next 16 hours and divide the maintenance evenly over 24 hours.
First 8 hours:
10 kg (Premorbid Weight) Child With 10% Hypotonic Dehydration (Sodium 115 mEq/L)
Give half of deficit in the first 8 hours and the remaining half over the next 16 hours; divide the maintenance evenly over 24 hours.
First eight hours:
10 kg (Premorbid Weight) Child With 10% Hypertonic Dehydration (Sodium 160 mEq/L)
Give half of the free water deficit + the total solute fluid deficit + solute sodium deficit + maintenance sodium and fluid divided over the first 24 hours.
Fluids:
Indications for Admission
Significant ongoing fluid losses and/or inability to tolerate oral fluids
Severe dehydration
Hypotonic or hypertonic dehydration
Bibliography
Colic
Colic, also referred to as paroxysmal fussing of infancy, is a benign, self-limited process whose etiology and pathogenesis are poorly understood.
Clinical Presentation
Infants commonly present around 2–3 weeks of age with paroxysms of inconsolable crying. The behavior peaks between 6–8 weeks and typically resolves by three months of age, although in 30% of cases the symptoms extend into the fourth and fifth months of life.
In mild cases, the fussiness occurs only in the evening or has some other regular diurnal pattern. Babies with colic may exhibit rhythmic kicking, grimacing, and flatus. However, vomiting, diarrhea, constipation, and failure to thrive are not characteristic of colic. The key feature of colic is that between episodes the infant appears comfortable and alert. The crying may not respond to the parents’ attempts at comforting or may cease only to resume when the infant is put down. Notably, the physical and neurologic examinations are normal. In the ED, the parents are concerned about the baby being ill, or they are exhausted and want relief.
Diagnosis
The key to making the diagnosis of colic is the parents’ statement that the infant is perfectly fine between paroxysms. However, several conditions other than colic can present with only fussiness or excessive crying. See Table 9.6 for the differential diagnosis of colic.
| Diagnosis | Differentiating features |
|---|---|
| Allergic colitis | Guaiac positive stools |
| Congenital glaucoma | Excessive tearing; abnormal red reflex |
| Congestive heart failure | Tachypnea and diaphoresis during feeding; failure to thrive |
| Constipation/diarrhea | Change in stooling pattern; anal fissure |
| Corneal abrasion | Conjunctival hyperemia, excessive tearing |
| Gastroesophageal reflux | Regurgitation; irritability related to feeds |
| Hair tourniquet syndrome | Swelling of a digit, penis, or clitoris |
| Incarcerated hernia | Mass in inguinal region |
| Infantile spasms | Attacks occur in clusters throughout the day |
| Infection/sepsis | Fever, vomiting, diarrhea, lethargy, or decreased feeding |
| SVT | Pallor, poor feeding |
| Testicular torsion | Swollen, erythematous hemiscrotum |
| Trauma/abuse | Swelling over affected site; decreased movement |
Perform a complete physical examination. If the baby cries during the examination, offer a gloved finger or nipple or place the infant in the prone position or over your shoulder. When distracted, the colicky baby will appear alert and will suck vigorously on a nipple or pacifier. Upon gentle palpation, the abdomen is soft and nontender.
ED Management
The goal of the ED examination is to rule-out other conditions that can present with colicky pain. Once the diagnosis is made, reassure the parents that the infant is not seriously ill and that colic is a self-limited phenomenon among otherwise well infants. There is no definite cure or universally accepted treatment for colic. Instead, the lack of a recognized etiology has led to the existence of a number of controversial remedies. Dispel any of the commonly held myths about colic, including that medications are beneficial, that infants are “spoiled” by excessive holding, and that colic is caused by parental inexperience and anxiety. Reassure the parents and offer them suggestions that may mitigate a crying attack, such as increased holding and rocking of the baby, more frequent feeding, use of a pacifier, and environmental changes (stroller ride, infant swing, car ride). Encourage the parents to burp the infant frequently during and after feeding if they are not already doing so. Finally, avoid antispasmodics and gripe water which have not been proven effective and may have side effects.
If there is suspicion of cow’s milk allergy, refer the family to a primary care provider who may decide to change to an elemental formula. Advise nursing mothers to consume a dairy- and soy-free diet until follow-up with the primary care provider.
Follow-up
Primary care follow-up within the week
Arrange for psychosocial support if the family can no longer cope with the crying
Bibliography
Related posts:
Full access? Get Clinical Tree
