Questions 17 - 24

17) Recommendations for automobile child passenger safety

All infants should ride rear-facing until they have reached at least 1 year of age and weigh at least 20 pounds. Once child is at least 1 year of age and weighs at least 20 pounds, he/she can ride forward-facing. Never place a child in a rear-facing car safety seat in the front seat of a vehicle that has a passenger air bag.

The child should stay in a car safety seat with a harness as long as possible before switching to a booster seat. You can tell when your child is ready for a booster seat when one of the following is true:

• Child reaches the top weight or height allowed for her seat with a harness. (These limits are listed on the seat and are also included in the instruction booklet.)
• Child shoulders are above the harness slots.
• Child ears have reached the top of the seat.

Booster seats are designed to raise the child so that the lap and shoulder seat belts fit properly. This means the lap belt lies low across the child's upper thighs and the shoulder belt crosses the middle of the child's chest and shoulder. Correct belt fit helps protect the stomach, spine, and head from injury in a crash. Children should stay in a booster seat until the adult seat belts fit him correctly. This is usually when the child reaches about 4' 9" in height and is between 8 and 12 years of age.

The child is ready to use a lap and shoulder seat belt when the belts fit properly. This means

• The shoulder belt lies across the middle of the chest and shoulder, not the neck or throat.
• The lap belt is low and snug across the upper thighs, not the stomach.
• He is tall enough to sit against the vehicle seat back with his legs bent without slouching and can stay in this position comfortably throughout the trip.

All children younger than 13 years are safest in the back seat.

Encourage parents to be a good role model and always wear their seat belt. This will help the child form a lifelong habit of buckling up.

18) Knowledge of age-related variations in renal function

2. At birth, the creatinine level of the newborn is similar to that of the mother and falls to the characteristic low level seen in neonates by about 7 to 10 days.

3. Compared with full-term infants, preterm infants waste salt excessively; their fractional excretion of sodium can be as high as 5% compared with less than 1% among older children.

4. Innormal individuals, as little as a 1% change in serum osmolality causes a significant change in serum antidiuretic hormone levels.

5. When using the Schwartz formula to compute glomerular ifitration rate at different ages, the K factor, which represents urinary creatinine per unit body weight, must be adjusted downward with age.

7. The concentrating capacity of the kidney reaches the adult value of about 1200 mOsm/kg at about 6 to 12 months.

AGE RANGE                                        CREATININE EXCRETION pmollkglday (mg/kg/day)

Full-term newborn                                                90 to 144 (10 to 16)

Infant                                                                     71 to 180 (8 to 20)

Child                                                                       71 to 195 (8 to 22)

Adult female                                                         97 to 177 (11 to 20)

Adult male                                                             124 to 230 (14 to 26)

AGE GROUP                                        GFR (MLIMIN/1.73 Mı)

25 weeks’ gestational age                                  2

Birth                                                                       Mother’s creatinine

Infancy to 3 yr                                                      18 to 26 (0.2 to 0.3)

4to7yr                                                                     26 to 44 (0.3toO.5)

8 to 10 yr                                                                53 to 71 (0.6 to 0.8)

Postpubertal females                                           71 to 80 (0.8 to 0.9)

Postpubertal males                                              80 to 106 (0.9 to 1.2)

Source: http://pedsinreview.aappublications.org

 

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19) Management of childhood stuttering

Stuttering that develops between ages 2 and 7 years is common and usually resolves on its own. Regardless of whether stuttering is expected to be a temporary condition, treatment can be helpful. Treatment usually includes parent counseling and speech therapy. Specific treatment varies depending on when and whether a child's stuttering is specifically diagnosed as:

• Normal disfluency, which likely will resolve on its own.
• Developmental stuttering (generally occurs because a child’s neurological system is not ready for all of the language that they are trying to say) often first appears around age 5 and generally requires treatment to improve.
• Acquired stuttering, which develops as the result of brain injury (usually from an accidental injury or a disease that affects the brain, such as Alzheimer's) or, less often, from severe emotional trauma.

Speech therapy for stuttering has a number of different approaches depending on factors such as the person's age, whether stuttering is likely to resolve on its own, and the severity of the problem. Usually, a speech-language pathologist also combines and expands on elements of parent counseling techniques. The two basic speech therapy methods used for treating stuttering are called indirect treatment and direct treatment.

• Indirect treatment focuses on creating a comfortable and relaxing environment in which the child's speech can improve naturally. A speech-language pathologist evaluates and monitors progress while observing the child and parents.
  
• Direct treatment is one-on-one personal interaction between a speech-language pathologist and a child who stutters. The speech-language pathologist teaches the child how to form words, speak slowly, and relax even while stuttering. The child can also practice these exercises outside of instruction time. The child also learns ways to eliminate the physical symptoms of stuttering, such as eye-blinking, and how to deal with the emotional difficulties that may result from speech problems.

Counseling for the child is often recommended when stuttering is complicated by additional problems, such as anxiety. It is also sometimes used when speech therapy has failed. Counseling and speech therapy are often used together for teenagers and adults who have developmental stuttering. The longer stuttering is left untreated, the more difficult it is to manage because additional problems frequently develop, such as low self-esteem. Speech therapy alone is unlikely to resolve these problems. Treatment of teens and adults takes longer and is generally less successful than for children.

Specialized therapies are needed for acquired stuttering that are usually specifically designed that often includes some combination of speech therapy, physical rehabilitation, and medicine.

Source: WebMD Stuttering – Treatment Overview

 

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Foreign body aspiration may appear as an acute onset of respiratory distress, or patients may have a silent presentation manifested by secondary complications. Most patients with foreign body aspiration present with an acute onset of choking, respiratory distress, cyanosis, severe coughing, and wheezing. A history of aspiration often is lacking, and patients may present days to weeks after the event. On examination, patients may have stridor, crackles, wheezing, decreased breath sounds in the affected lung, or normal results on pulmonary physical examination.

Typical symptoms of complete airway obstruction that occurs while a person is eating a meal include severe respiratory distress and the inability to speak or cough. Individuals typically place their thumbs and index fingers around their neck.

Patients with partial airway obstruction may present with a sudden onset of coughing, difficulty in breathing, wheezing, or stridor while eating a meal. Unfortunately, a history consistent with foreign body aspiration is usually available in only 70% of patients. After the acute episode of airway distress, patients may continue to experience episodes of persistent coughing and wheezing, or they may become asymptomatic. Moreover, some patients experience recurrent episodes of pneumonia in the same topographic area. Other patients develop complications, such as hemoptysis, bronchiectasis, and bronchial stricture.

MDMA (3,4-methylenedioxymethamphetamine) continues to gain popularity as a drug of abuse, particularly among adolescent and young adult party-goers at "raves" and "circuit parties," due to its capacity to elicit feelings of euphoria, wakefulness, intimacy, and disinhibition.

Peak effects of MDMA toxicity occur within two hours of ingestion and typically last four to six hours. Concentrations of MDMA contained in illicitly produced pills vary widely. Major toxicity and death may occur after ingestion of a single tablet. MDMA intoxication can cause a myriad of dangerous effects including severe hypertension, hyperthermia, delirium, psychomotor agitation, and profound hyponatremia. Potential life-threatening complications of these effects include intracranial hemorrhage, myocardial infarction, aortic dissection, disseminated intravascular coagulation, rhabdomyolysis, seizure, and serotonin syndrome.

· The differential diagnosis for MDMA intoxication includes other sympathomimetic drugs of abuse, such as cocaine, amphetamine, and methamphetamine, and anticholinergic toxicity. Hypoglycemia, electrolyte disorders, intracranial hemorrhage, and infection should also be considered

· Routine laboratory evaluation of the poisoned patient should include the following: Fingerstick glucose, Acetaminophen and salicylate levels, ECG, and UPT in childbearing age women

· For patients in whom significant toxicity related to use of MDMA is suspected, the clinician should also obtain the following :

- Basic serum electrolytes; if hyponatremia is present, a serum osmolality is recommended
- Creatine kinase and urine myoglobin
- Serum creatinine
- Serum aminotransferase concentrations
- Coagulation studies (ie, aPTT, PT, INR, platelet count, d-dimer)

The brown recluse spiders in the United States are known as fiddlebacked or violin spiders because of a dark violin pattern in the front portion of the body. They have only three pairs of eyes and measure 2 to 3 cm in diameter. Brown recluse spiders live in human dwellings and hide during the day in baseboards, ceiling cracks, or behind furniture or undisturbed clothing.

Brown spider bites may go unnoticed, cause a mild local reaction, or in a few cases cause a severe local reaction (necrotic arachnism). They may also cause loxoscelism, a syndrome associated with hemolysis and death.

Venom — almost all of the crude extracts of the Loxosceles venom is hyaluronidase spreading factor. Sphingomyelinase-D, called loxosotoxin, is a responsible for lysis of red blood cells and platelets. Both necrotic arachnism and loxoscelism result from the absorption and systemic effects of loxosotoxin contained in the venom. However, the amount of loxosotoxin in one spider bite is too small to account for the extensive Coombs-negative hemolytic syndrome seen in cases of severe loxoscelism; unknown concomitant factors may be contributing. Loxosotoxin is antigenic. Thus, subsequent bites by brown recluse spiders are usually less severe than the initial bite.

Clinical reactions — A study of 111 patients who suffered brown spider bites found that the majority (81 percent) had erythematous, violaceus, or hemorrhagic discoloration at the site of the bite; 41 percent had central necrosis of the lesion. The initial lesion occurs within ten minutes of the bite and consists of a clean infarction of the skin that is free of inflammation in the center but has cellular infiltrates in the margins. Clinically this is manifested as a sinking blue macule with a halo of surrounding erythema. Lesions are usually painful, with loss of light touch sensation in the center.

Brown spider bites typically are localized to the upper arm, thorax, or inner thigh. Hand or face (uncovered areas) bites are exceedingly rare. The lesion can enlarge to involve an entire limb, particularly in children. Fever, local burning pain, and an erythematous rash may persist for several days. Necrotic arachnism is associated with extensive scabbing, the development of necrotic tissue, and very slow healing.

Loxoscelism is characterized by fever (up to 40ºC, 104ºF), chills, vomiting, and joint pain with hematuria and hemolytic anemia. The hemoglobin concentration can be reduced to one-half the normal range within 24 hours of the bite. Anuria develops with extensive hemolysis; acute renal failure is rarely seen. Clotting systems remain intact in most cases, although coagulation disorders with consumption of fibrinogen, petechiae, and thrombocytopenia may occur. The presence of black urine associated to nausea, vomiting and malaise should alert to the presence of hemolysis.

23) Recognition of the symptoms of acquired disaccharidase deficiency

Disaccharidase Deficiency

Starches and the disaccharides sucrose and lactose are the most important dietary carbohydrates. Dietary disaccharides and oligosaccharide products of pancreatic amylase action on starch require hydrolysis by intestinal brush border disaccharidases before absorption takes place. Because disaccharidases are located on the luminal surface of intestinal enterocytes, they are susceptible to mucosal damage. Many conditions cause secondary disaccharidase deficiency, with lactase usually most severely depressed.

Secondary (Acquired) Lactase Deficiency

The most common mechanism producing secondary lactase deficiency is small intestinal injury due to viral infection. The deficiency is usually self-limited, lasting days or, at most, weeks after recovery from infection. With Lactose ingestion clinical findings include diarrhea, gassy distention, and abdominal pain. The stools can be frothy, with a pH below 4.5 owing to the presence of organic acids. Vomiting is common.

Patients respond to a reduction of dietary lactose. Tolerance for dietary starch and sucrose is normal. Lactase extracted from Aspergillus and Kluyvera species can be added to milk products or taken with meals to enhance lactose hydrolysis

Intestinal mucosal damage tends to reduce the activity of all disaccharidases. Signs of sucrose intolerance are usually masked by the more striking symptoms of lactose intolerance. Infectious diarrhea is the most common cause of secondary sucrose intolerance.

Source: www.accessmedicine.com on disaccharide deficiency

 

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24) Physical findings of an orbital floor fracture

Orbital floor fracture — Fractures of the floor of the orbit, sometimes known as "blowout fractures," typically occur when a small round object, such as a baseball, strikes the eye. Experimental evidence suggests that orbital floor fractures may be caused by one or both of the following mechanisms:

• Increased intraocular pressure as the result posterior displacement of the globe (hydaulic theory) 
  
• A direct blow to the infraorbital rim

Among children, the floor of the orbit is more flexible. Consequently, it may fracture in a linear pattern that snaps back to create a "trap-door" fracture. In adults, the floor of the orbit is thinner and more likely to shatter when exposed to force.

A significant consequence of fractures of the orbital floor is entrapment of the inferior rectus muscle and/or orbital fat. Ischemia and subsequent loss of muscle function may occur either because of entrapment of muscle within the fracture fragment (more likely in children), or as the result of edema and hemorrhage of muscle and extraocular fat that have prolapsed through the fracture into the maxillary sinus (more likely in adults).

Enophthalmos (the eye is receded into the orbit) may develop when the globe is displaced posteriorly in association with an orbital floor fracture and prolapse of tissue into the maxillary sinus. Orbital dystopia (the eye on the affected side is lower in the horizontal plane than the other) may occur because entrapped muscle and orbital fat pull the eye downward.

Injury to the infraorbital nerve (resulting in decreased sensation along the cheek, upper lip, or upper gingiva) may occur as the result of an orbital floor fracture.