860

macroscopic haematuria in children is commonly associ-ated with glomerular disease-two-thirds of patients inreferral practice 7,8 or 10% of unselected patients.9 9How should the clinician react to a positive dipstick

test? Inquiry may elicit a story of previous macroscopichaematuria, suggesting recovering acute nephritis, or apedigree of familial nephritis. Physical examinationmust include the genitalia and abdomen, and a searchfor oedema; rare associations (aniridia and nephroblasto-ma) should be recalled. Urine microscopy will confirmerythrocyturia; and the finding of casts or dysmorphicred cells, perhaps by phase-contrast microscopy,1O willsuggest a renal origin. Bacteriuria and pyuria indicateinfection and the need for urine culture. Proteinuria (1+or more by dipsticks) should be quantified by a timedcollection, and orthostatic proteinuria should be ruledout. Renal function can be estimated from the serumcreatinine." If these tests are normal the child and his

parents can be told that the finding is probably unimpor-tant, an annual urine’ check and blood-pressuremeasurement being all that is required. If macroscopichaematuria or proteinuria develops, this will demandfurther assessment. Urography should be done spar-ingly, mainly on children with other symptoms, and cys-

toscopy almost never. Opinions differ on the manage-ment of children with MH and persistent proteinuria orraised serum creatinine. Some paediatricians are againstrenal biopsy because the kidney is likely either to be nor-mal or to show a nephropathy for which there is noestablished therapy; but this policy may have to changein the light of new ideas on specific treatment for glo-merulonephritis.12 Three conclusions can be drawn fromthe Helsinki study. Firstly, widespread testing for MH insymptomless children cannot be recommended as a use-ful screening procedure for progressive renal disease.Secondly, that investigation of otherwise normalchildren with MH should be restrained. And, lastly, thatthe sensitivity of dipsticks for haemoglobin should not beincreased (as was the case in this study); it should be un-changed, or reduced.

POST-ASTHMATIC PSEUDO-POLIO IN CHILDREN

IN 1974 Hopkins’ reported from Australia 10 childrenin whom a poliomyelitis-like illness developed a few daysafter an exacerbation of asthma. Since then, similarcases have been reported from England,2,3 the U.S.A.,4

7. Glasgow EF, Moncrieff MW, White RHR. Symptomless hæmaturia in Child-hood. Br Med J 1970; ii: 687-92.

8. Wyatt RJ, McRoberts JW, Holland NH. Hematuria in childhood: Signifi-cance and management. J Urol 1977; 117: 366-68.

9. Inglefinger JR, Davis AE, Grupe WE. Frequency and etiology of gross hema-turia in a general pediatric setting. Pediatrics 1977; 59: 557-61.

10. Birch DF, Fairley KF. Haematuria: glomerular or non-glomerular. Lancet1979; ii: 845-46.

11. Counahan R, Chantler C, Ghazali S, et al. Estimation of glomerular fil-tration rate from plasma creatinine concentration in children. Arch DisChild 1976; 51: 875-78.

12. Collaborative Study of the Adult Idiopathic Nephrotic syndrome. A con-trolled study of short-term prednisone treatment in adults with mem-branous nephropathy. N Engl J Med 1979; 301: 1301-06.

1. Hopkins IJ. A new syndrome: poliomyelitis-like illness associated with acuteasthma in childhood. Aust Paediatr J 1974; 10: 273-76.

2. Danta G. Electrophysiological study of amyotrophy associated with acuteasthma (asthmatic amytrophy). J Neurol Neurosurg Psychiatry 1975; 38:1016-21.

3. Ilett SJ, Pugh RJ, Smithells RW. Poliomyelitis-like illness after acute

asthma. Arch Dis Childh 1977; 52: 738-40.4. Shapiro GG, Chapman JT, Pierson WE, Bierman CW. Poliomyelitis-like ill-

ness after acute asthma. J Pediatr 1979; 94: 767-68.

and Sweden,s and 3 additional cases from Australia.’There can be no doubt that this constitutes a real, if un-- common, clinical entity. It is important because there isalways severe, residual, flaccid weakness of the affectedlimb or limbs; because the paralysis may be wronglyattributed to some therapeutic mishap (e.g., intravenoustherapy); and because of the mystery surrounding itscausation and prevention.The ages of the affected children have ranged from 1to 11 years. Almost twice as many males as females havebeen reported. All have been fully immunised againstpoliomyelitis, most with Sabin (live) vaccine but at leastone5 with Salk (killed) vaccine. All children were knownasthmatic subjects, some also with eczema. The attacksrelated to the polio-like illness have been severe enoughto need hospital admission, intravenous therapy, and, ina few cases, assisted ventilation.The neurological troubles start 4-11 days after the

onset of the wheezing, the mode being 5 days. Usuallyonly one limb is affected, the arm more commonly thanthe leg. The left side seems more vulnerable than theright. The child first complains of pains in the affectedlimb(s) and the nerves may be tender. Soon afterwardsflaccid weakness is apparent, which is often severe.

There are no sensory changes. Clinical and neurophysio-logical examinations point to a lesion in the anteriorhorn cells, or possibly in the motor roots or plexuses.The condition is not a peripheral neuropathy. Thecerebrospinal fluid may be normal, but lymphocyte andprotein content have been increased in some cases. Sub-sequently there may be a little improvement, but resi-dual weakness and muscle wasting are usually striking.

The- xtiology is obscure. Viruses have been recoveredfrom a few affected children (adenovirus type 9, echo-virus type 18, varicella virus, Coxsackievirus B5) butsignificant rises in viral antibody titres have not beendetected. Manson and Thong6 did extensive immunolo-gical studies on their 3 patients. All had raised IgM andIgE levels, 2 had low T-cell numbers, and 1 had in addi-tion impaired neutrophil chemotaxis and no detectableantibodies to types 2 and 3 poliovirus after full Sabinimmunisation (type 1 titre 1:24). These findings aredifficult to interpret because the children are atopic sub-jects.The fact that this syndrome has so far been described

only in association with asthma, and the striking clinicalresemblance to anterior poliomyelitis, suggest a possibleinteraction between some neurotropic agent(s) and analtered immunological state. The fact that so far all

reported cases have been fully immunised against polio-myelitis means little because there are so few of them.It would nevertheless be interesting to know whetherthis condition occurs in unimmunised children. Polio-virus antibody titres have not risen in association withpseudopolio in any of the children tested.

This condition could give rise to medicolegal disputes.If an arm becomes paralysed a few days after it has beenused for an intravenous infusion or injection, a cause-and-effect relation may be suspected. Electrophysiologi-cal studies can be helpful in identifying the site of thelesion.

5. Blonquist HK, Björkstén B. Poliomyelitis-like illness associated with asthma.Arch Dis Childh 1980; 55: 61-74.

6. Manson JI, Thong YH. Immunological abnormalities in the syndrome ofpoliomyelitis-like illness associated with acute bronchial asthma (Hopkins’syndrome). Arch Dis Childh 1980; 55: 26-32.