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Elevated serum levels of neuron-specific enolase and S-100 are correlated with poor prognosis. After 24­48 hours of severe anoxia, a loss of distinction between gray matter and white matter at the level of cortex and basal ganglia reflects cytotoxic edema. It should be considered in patients with unexplained coma, with or without convulsive activity, after cardiac arrest. Serious dysfunction of the neuromuscular system may lead to hypoventilation and hypercapnia, with respiratory failure requiring mechanical ventilation. Clinical Findings the pattern of weakness may be helpful in localizing the underlying disorder. Proximal musculature may be more adversely affected, but distal weakness is common. Sensation may be impaired but is often difficult to assess in critically ill patients. Cranial nerves are not typically affected except for bilateral facial weakness, which may be difficult to recognize in a ventilated patient. Myasthenic crisis is usually triggered by acute illness or new medication (see Chapter 22). It is crucial to recognize signs of respiratory weakness and the need for intubation and mechanical ventilation before an acute decompensation. Delayed intubation contributes to the development of aspiration pneumonia (Table 25­4). Patients who have been exposed to neuromuscular junction­blocking agents are at risk for prolonged effects of these agents. Electromyography shows signs of denervation and abnormal compound muscle action potentials. Nerve conduction studies may confirm axonal neuropathy but are often unreliable in this setting. Because management consists of physical therapy for both syndromes, muscle biopsy is reserved for specific settings. As a preventive strategy, paralytic agents should be used judiciously and sparingly, particularly in combination with high-dose corticosteroids. Urgent commencement of treatment is of the essence; when antibiotics are initiated after 6 hours from arrival for care (generally due to delay in performing lumbar puncture) the prognosis is much worse. These cytokines, such as tumor necrosis factor and interleukin-1, break down the blood­brain barrier, leading to edema and cell death. The capsule helps evade complementmediated efforts to kill and phagocytose the bacteria, and vesicles released by the outer membrane of bacteria divert the immune response. It is associated with morbidity in up to 50%, the most serious being cerebral edema with depression of consciousness and septic shock; mortality rates up to 20% have been reported. Dosagea Causative Organism Neisseria meningitides (meningococcus; gram-negative pairs) Drug (2-wk course) Penicillin G or Ampicillin or Ceftriaxone (if penicillin resistant) or Cefotaxime or ceftizoxime Rifampin (oral) or Ciprofloxacin (oral) Children 50,000 units/kg q 4 h Neonates: 0. Special entry mechanisms include thrombosed veins in the presence of extracranial infection such as otitis or mastoiditis, which allow retrograde transmission of infection. After nasal, mastoid, sinus, or cranial surgery, or penetrating head trauma, violation of the dura allows a passageway for bacterial entry of those colonizing the skin or sinuses. Foreign bodies within the brain such as ventricular drains or shunts, Ommaya reservoirs, and deep brain and corticography electrodes can also become infected after even transient bacteremia. These can lead to hydrocephalus or increased intracranial pressure and herniation. Stroke may be the consequence of arteritis as large blood vessels cross through the exudate at the base of the brain. In the United States, the majority of meningitis is caused by S pneumoniae (58%), followed by group B streptococci (18%), meningococci (13. Prevention Vaccination programs against common pathogens such as H influenzae and N meningitidis were expanded to infants in 1990, and in 2000 S pneumoniae was added. It is important to adhere to recommended vaccination schedules throughout infancy and childhood as effectiveness usually wanes after 1 year. Public health vaccination efforts in the United States and elsewhere have led to a significant decline in the incidence of meningitis (both unexplained and due to the above organisms). Median age of infection increased from 15 months to 25 years with more patients presenting over age 60.

While there is theoretical, laboratory and anecdotal support for these treatments there is, as yet, little objective evidence of clinical benefit. Metabolic Disorders Clinical scenario A 3 month old presents having had a viral infection with lethargy and sweating. On examination of the abdomen a 5 cm lever edge is palpable below the right costal margin. Types of lesion Papule Nodule Macule Plaque Wheal Vesicle Bulla Elevated lesion < 0. Pinpointwhitepapulesoverthenose,cheeks,upperlip,forehead Around 40% of infants also have minute 1­2 mm follicular epidermal (keratin filled) cysts (milia), which resolve in a few weeks. Itchiness Dryskin Hyperlinearityofpalmsandsoles Dennie­Morganfold(foldundereyes,notspecificto eczemabutindicativeofatopy) n Dryirritatedswolleneyelids n n n n 290 Figure 17. Treatment First-line therapy Generaladvice Dermatology Detailedadviceabouteczema,environmentalfactorsandhowtousetopical treatments Keepnailsshort Useonlyloosecottonclothing Stopadultssmokinginthehouse Reductionoftriggers Avoidallergens. Topical steroids: groups and side effects Potency Mild Moderate Potent Very potent Side effects n n n n n Thinning of skin (atrophy) Petechiae Telangiectasiae Striae distensiae Growth retardation (if used to excess) Example Hydrocortisone Eumovate Betnovate Dermovate Second-line therapy Topicalimmunomodulator iveniftopicalsteroidsareinsufficient G (tacrolimusorpimecrolimus) 292 Foodallergymanagement Wetwrapsandbandages Insomechildrencertainfoodsworseneczema(onsetmayalsobeclearly relatedtointroducingcertainfoods). Lesions of acne n Comedones(plugsofsebaceousmaterial withinhairfollicleunit) (opencomedones=blackheads;closed comedones=whiteheads) n Papules,pustules n Nodules,cysts n Scars Treatment Topical Antibacterialandkeratolytic,e. Thesemaycause: n Noreactioninyounginfants,or n Papularurticaria n Also,commonestcauseofblistersinchildren Infections Figure 17. Overthe backtheyformasymmetricalpatternalong theriblinessaidtoresemblethefoliageofa Christmastree n Causeisunknownbutpossiblyviralandit resolvesspontaneouslyafter6­8weeks n Mildtopicalsteroidscanbeappliedtospeedup resolution Figure 17. Acommoncauseis Trichophyton tonsurans(thisspeciesinvadesthehairshaft) Tinea corporis(verycommon) Scalyredannularlesionsontrunkand/orlimbs Trichophyton rubrumisacommoncause Management n Takefungalskin scrapingsorhairpluckings(intineacaptitis)formicroscopyandthenfungalculture n Tinea corporis ­topicalantifungalfor2­4weeks,e. Typicaltargetlesionsarenotalwaysseen 300 n Notreatmentisrequiredandtherashresolves spontaneouslyin2­3weeks,butoftenrecurs n Secondarytoherpes simplex virus infection(cold sores­mostcommoncause),drugs,e. Ichthyosis vulgaris n Commonmildichthyosis,incidence1in300­ 500 n Dryroughskin,withhyperlinearpalms n Treatedbyregularmoisturizing n Associatedwithanincreasedincidenceof atopiceczema Figure 17. Three days later she develops a vesicular rash which is painful and on discussion with her family it is apparent that she has had contact 14 days previously with a child with chicken pox. There are different types of haemoglobin, which have different affinities for oxygen and therefore are useful at different stages of development. Haemoglobin is composed of four polypeptide chains, each with a haem group attached, and it is a variation in the polypeptide chains that differentiates the types of haemoglobin. The switch from fetal haemoglobin to adult haemoglobin production occurs by 3­6 months of age. The clinical features are due to the anaemia, increased requirements and increase in red cell breakdown products (causing jaundice). Intravascular haemolysis (destruction of red cells within the circulation) occurs in some conditions and causes specific features. This shape means they are unable to pass through the splenic microcirculation, and so die prematurely. Clinical features n Very variable even within families n Neonatal jaundice n Symptoms of mild haemolytic anaemia, especially splenomegaly, pigment gallstones and aplastic or anaemic crises with parvovirus infection n May be asymptomatic 314 Investigations Blood count Film Membrane studies Other Management n n n No treatment if mild Folic acid supplements for haemolysis Splenectomy after childhood if severe anaemia requiring regular transfusions or causing impaired growth Anaemia Anaemia (may be mild) Reticulocyte count 5­20% Microspherocytes Defect in membrane protein Autohaemolysis, bilirubin Glucose-6-phosphatedehydrogenasedeficiency X-linked recessive condition; females mildly affected. The gene is selected for because the carrier state protects against falciparum malaria. Defective enzyme activity results in a susceptibility of the red cell to acute haemolysis with oxidant stress. Causes Primary Secondary Fanconi anaemia Idiopathic (most cases) Drugs: Regular effect. HbS is insoluble in low oxygen tensions and polymerizes as long fibres which result in the red cells becoming sickle shaped. Clinical features are due to: n n Anaemia ­ Hb 6­9g/dL, reticulocytes 5­15% Intermittent crises Haematology Cerebral (stroke) Chest (Sickle cell syndrome) ­ severe life-threatening Bone (commonest) Liver Kidney Heart Spleen (result in autosplenectomy usually by age 5 years) Dactylitis (hand­foot syndrome) (digital infarcts occur usually in young children, resulting in fingers and toes of differing lengths) Figure 18. These are vascular-occlusive episodes precipitated by cold, hypoxia, infection or dehydration. This is haemolysis and it usually accompanies a painful crisis n Acute sequestration. A sudden fall in the Hb and reticulocyte count is seen Infection these children are at high risk of infection with encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae B, meningococcus and salmonella species.

Syndromes

• Get drunk
• Amount swallowed
• Stop talking in mid-sentence and start again a few seconds later
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• Do you have other symptoms like eye discharge, burning, or itching? Nausea or vomiting? A headache?
• Peeling ointments containing salicylic acid on patches of thick skin