ST. JMC JOURNAL OF MEDICINE ISSN 0970-4221 VOL. IV NO. 3&4 DECEMBER 1991
Item
- Title
- ST. JMC JOURNAL OF MEDICINE ISSN 0970-4221 VOL. IV NO. 3&4 DECEMBER 1991
- extracted text
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COMMUNITY HEALTH CELL
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Koramtngali*
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India
ISSN 0970-4221
ST. JOHN'S MEDICAL COLLEGE
JOURNAL OFJVIEDICINE
VOL IV No 3 & 4
EDITORIAL
Oct-Dec 1991
43
NEPHROLOGY SYMPOSIUM
Chronic Renal Failure
45
Urinary Tract Infection in Children
55
ORIGINAL ARTICLE
Attenuation of the Haemodynamic response to
Laryngoscopy and Tracheal Intubation
59
SELECTED SUMMARIES
-
Sleep Apnea Syndrome
REVIEW
-
History of Surgery - A Brief Review
04
EDITOR-IN-CHIEF
1
INFORMATION FOR CONTRIBUTORS
Ashley. J. D'Cruz
Submitting the Manuscript
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• communications.should be addressed to the Editor, Alumni Office, St. John's Medical College,
Bangalore-560 034.
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Ravi C. Nayar
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REFERENCES
PUBLISHER
Prof. A.F.A. Mascarenhas
Principal
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Kurpad AV, Shetty PS: Dietary Fibre and the colon. St.John's J Med, 1988;1:5-12.
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Complete book
Gallagher JR: Medical Care of the Adolescent (ed 2). New York, Appleton, 1966; pp 208-215
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St. John’s Medical College Journal of Medicine
EDITORIAL
MANAGEMENT OF BENIGN OESOPHAGEAL STRICTURES
Benign strictures of the oesophagus are difficult problems in surgery. The problems faced by patients with such strictures
are no less serious than malignancies of the oesophagus and they suffer equally from sialorrhoea, inanition and regur
gitation leading to aspiration pneumonia. These problems are greater in patients with benign strictures, particularly those
with corrosive stricture, because most patients are young and expected to live long. This is precisely the reason why
energetic treatment, often by surgical means, is strongly advocated for these lesions.
Benign strictures of the oesophagus are caused by a variety of conditions. Notable amongst these are corrosive strictures,
peptic strictures following reflux oesophagitis, injuries (violence or iatrogenic), infective oesophagitis (bacterial, viral
and fungal), non-infective granulomatous lesions of the oesophagus, Barett’s oesophagus etc. Corrosive and peptic
strictures are by far the commonest causes accounting for almost 95% of the case of oesophageal stricture. While peptic
strictures are more common in developing countries including India. Not withstanding the aetiological difference, one
element which is common to both is submucosal injury leading to scarring and resultant stricture. The extent of stricture
following corrosive injuries may be either a small segment, a long segment, or even multiple sites. It is not unusual to have
patients with burns leading to strictures of the entire upper aerodigestive tract causing contracted oral cavity, hypopharynx,
laryngeal stenosis etc. Some patients live permanently with a tracheostomy.
The peptic strictures on the other hand are restricted usually to the lower oesophagus. While most strictures are more than
3 mm in diameter extending for 3 cms, about 10% of peptic strictures are worse and they can be termed severe. Although
acid reflux is universal, associated peptic ulcer is seen in only 15-25% of the patients. Occasionally patients with hiatus
hernia also develop stricture due to associated reflux oesophagitis.
As a result of stricture formation due to fibrosis the oesophagus gets shortened with consequent decrease in lower oeso
phageal sphincter pressure resulting in more reflux and further stricture.
Once the stricture forms, patients with both corrosive injuries and reflux oesophagitis present with dysphagia essentially
to solids in the beginning and later to liquids. Patients find it increasing difficulty to swallow even their own saliva leading
to aspiration pneumonia. While history of corrosive ingestion is always present in corrosive strictures, history of reflux like
heart burn, soar eructation and chest pain is in frequently seen in the peptic stricture group. In patients with corrosive
strictures of the oesophagus, associated features of gastric outlet obstruction may be seen particularly in those with a
history of acid ingestion.
The mainstay of diagnosis of oesophageal strictures is a barium swallow X-ray. It demonstrates the site of stricture and its
extent. Oesophagoscopy is required to assess the lumen and the feasibility of dilatation. At times, a doubtful lesion may be
biopsied to exclude malignancy which may complicate such strictures. It also determines the presence of reflux
oesophagitis, presence of peptic ulcer disease and evidence of gastric outlet obstruction. In doubtful cases if facilities are
available, oesophageal manometry should be done to rule out motor disorders of oesophagus. Oesophageal pH monitoring
may be of use to confirm gastro oesophageal reflux. A Radioisotope meal can be a noninvasive method of diagnosing
gastro oesophageal reflux.
The aim of treatment is to relieve dysphagia, prevent starvation, avoid sialorrhoea and aspiration and to abolish reflux if
present.
The treatment in most cases of stricture is dilatation. In cases of peptic strictures one is almost always able to dilate, surgery
is very rarely needed for such strictures. Once dilated most strictures will remain dilated provided reflux and associated
oesophagitis is kept under control with postural and antireflux measures including diet and drugs (essentially antacid and
H2 receptor blockers). Overthe years rigid dilators (Metal, gun elastic or Teflon) are used for such purposes without guide
wires. In recent time, however, such rigid dilators can be passed using guidewires like Eder-Puestow dilators or Celestin dilator.
While only 2 passages are necessary using Celestin dilators, repeated insertion of spring coiled dilators are necessary
if Eder-Puestow dilators are used. Some authorities feel satisfied with the use of non-rigid dilators like mercury filled dilators,
pneumatic dilators or hydrostatic dilators. Irrespective of the type of dilators used, dilatation should continue till dysphagia
disappears. Thereafter, dilatation should continue once a week or once in 2 weeks. Most strictures do not require more than
3 sittings of dilatations.
Oct - Dec 1991
43 —
St. John’s Medical College Journal of Medicine
When surgery is imperative due to recurrence of strictures with or without reflux oesophagitis, operative dilatation or local
resection of the strictured segment coupled with one of different antireflux operations is performed. Because of its simplicity
we usually perform Nissen’s fundoplication. instead of complete excision some authortities advocate through and through
division of the stricture convered with a Thai’s patch. If performed properly most patients remain well with postural and
dietary adjustments and drug therapy whenever necessary. An obstinate case may require total oesophagectomy as a last
resort.
Results of dilatations for corrosive stricture are not universally good. Appleberg reported 86% success rate with
14% perforation. Oakes on the other hand recommend early surgery because extensive strictures need prolonged
dilatation. The present author however, takes a balanced view recommending dilatation for short segment solitary
strictures reserving surgery for multiple, long segment, very narrow and tortuous strictures because perserverance with
dilatation in these groups amounts to procrastination. We therefore, consider surgery essential if dilatation is difficult
or becomes increasingly difficult during subsequent siltings. The procedure can be so difficult and troublesome that a
significant number of patients decline to undergo dilatations and ask for surgical treatment. Perforations produced during
dilatation is a definite .indication for surgical treatment. In this context it may be mentioned that even if dilatation succeeds,
patients may not swallow normally because strictures developing from deep muscular injuries loose their persistaltic
activities and lower oesophageal sphincter pressure. Both these factors may worsen the patients swallowing ability.
Furthermore, such patients may develop reflux oesophagitis with or without hiatus hernia often responsible for further
stricture formation which may be denser than before. In addition if dilatation is continued for an unduly long period, patients
particularly children, can suffer from growth retardation and psychological handicap. When surgery is advocated,
oesophageal bypass is commonly practised. However, for fear of malignancy (the incidence of which is a matter of doubt)
one may remove the damaged oesophagus with or without thoracotomy and using stomach, colon or jejunum (in that order)
as oesophageal replacement. The problem of surgery for corrosive strictures is the mortality which is upto 8% in the world
literature. We at AllMS have 4% mortality in a series of 45 extensive strictues treated by surgery alone. The procedure may
be associated with various complications but when done carefully these can be avoided.
The other problem of oesophageal bypass or replacement is stricture at the anastomosis due to fibrosis of proximal
oesophagus (as a result of corrosive burn). This is a difficult problem to tackle and we have introduced a simple, effective,
self dilatation technique for the managment of such strictures with good results.
Dr. T. K. Chattpopadhya
Department of Surgery,
AllMS,
New Delhi
44
VOL IV No 3&4-----
NEPHROLOGY SYMPOSIUM
St. John’s Medical College Journal of Medicine
CHRONIC RENAL FAILURE
K. USHA
uremia, leading to retention of urea and other metabolic end
products in blood .5
INTRODUCTION
Chronic renal failure is a functional diagnosis characterized
by a progressive and irreversible decline in glomerular
filtration rate. Many forms of renal injury associated with
permanent nephron loss progress inexorably to chronic
renal failure. Reduction of renal mass causes structural
and functional hypertrophy of remaining nephrons and is
due to adaptive hyper filteration mediated by increase in
glomerular capillary pressure and flow*1. Eventually these
adaptations prove “maladaptive" in that they predispose
to glomerular sclerosis, an enhanced functional burden on
less affected glomeruli, leading in turn to their ultimate
destruction (Fig 1)2.
Glomerulonephritis is the most common cause of chronic
renal failure and younger people are overwhelmingly affected
in tropics as compared to Western Europe.3 Histological
diagnosis in 576 renal biopsies at Jaslok Hospital, Bombay
revealed primary glomerulonephropathy 74 (membrano
proliferation 20, acute endocapillary 22, mesangial 26),
interstitial nephritides 8, hypertension 8, systemic disease
7.4 The other major etiologies of chronic renal failure are
listed in (Table 1).
TABLE-1: Causes of Chronic Renal Failure
Glomerulonephritis
Pyelonephritis
Obstructive nephropathy
Diabetes Mellitus
Hypertension
Polycystic kidney disease
Other interstitial nephritis
Congenital abnormalities
Unknown aetiology
PATHOPHYSIOLOGY
TIONS
AND
CLINICAL
MANIFESTA
Uremia, is a term generally applied to the clinical syndrome
observed in patients suffering from profound loss of renal
function. The failure of renal excretory function, biosyn
thetic processes and hormonal regulation6 results in
i
j
I
l
K. USHA MD
LECTURER IN NEPHROLOGY
ST.JOHN'S MEDICAL COLLEGE AND HOSPITAL
BANGALORE - 560 034
Oct - Dec 1991
The presentation and severity of signs and symptoms of
uremia often vary greatly from patient to patient, depending,
at least in part, on the magnitude of the reduction in
functioning renal mass as well as the rapidity with which
renal function is lost. Azotemia, defined as a rise in blood
urea and creatinine the patient being asymptomatic,
occurs when total glomerular filteration rate (GFR) falls
below 50 percent of normal. The presence of sudden stress,
in an asymptomatic patient, such as intercurrent infection,
urinary tract obstruction, dehydration, or administration of
nephrotoxic drugs, may compromise renal function further
leading to signs and symptoms of overt uremia. The patient
develops overt renal failure when total GFR is below 20 to
25 percent of normal.
The uremic syndrome results from derangements of function
in many systems of the body, and the specific symptoms
may vary from patient. The manifestations of uremic
syndrome are listed briefly in Table 2.
TABLE-2 : Manifestations of the Uremic Syndrome
Neurologic:
Central
Daytime drowsiness and a tendency to sleep
Progressing to increasing obtundation and eventual coma
Decreased attentiveness and cognitive tasking
Imprecise memory
Slurred speech
Asterixis and myoclous
Seizures
Disorientation and confusion
Pheripheral:
Sensorimotor peripheral neuropathy, often with burning
dysesthesia
Restless leg syndrome
Increased muscle fatigatility and muscle cramps
Cardiovascular :
Accelerated atherosclerosis
Cardiomyopathy
Pericarditis
Hypertension
Pulmonary :
Atypical pulmonary edema
Pneumonitis
Fibrinous pleuritis
45 —
St. John’s Medical College Journal of Medicine
Gastrointestinal:
Anorexia progressing to nausea and vomiting
Stomatitis and gingivitis
Parotitis
Peptic ulcer diathesis
Gastritis and duodenitis
Enterocolitis
Pancreatitis
Ascitis
Dermatologic :
Pruritus
Dystrophic calcification
Changes in skin pigmentation
Hematologic :
Anemia
Altered neutrophilic chemotaxis
Depressed lymphocyte function
Bleeding diathesis with platelet dysfunction
Endocrinologic :
Secondary hyperparathyroidism
Carbohydrate intolerance due to insulin resistance
Type IV hyperlipidemia
Altered peripheral thyroxine metabolism
Testicular atrophy
Ovarian dysfunction with amenorhoea, dysmenorhoea,
dysfunctional
Uterine bleeding, cystic ovarian disease
Ophthalmic :
Conjunctival or corneal calcifications
Fluid and Electrolyte Disturbances :
Hypervolemia, hypovolemia
Hyponatremia, hypernatremia
Hyperkalemia, hypokalemia
Metabolic acidosis
Hyperphosphatemia, hypophosphataemia
Hypercalcemia, hypocalcemia
Hypermagnesemia
Hyperuricaemia
Potentially toxic compounds that accumulate in renal
failure and may be responsible for the uremic
symptoms
Urea
Phenols
Indoles
Skatoles
Hormones
Polyamines
Trace elements
46
Pyridine derivatives
Guanidino compounds
B2 microglobulin
Aliphatic amines
Hippurate esters
Middle molecules
Aromatic amines
Water, Electrolyte, and
Uremia :
Acid-Base
Metabolism
in
Renal and extrarenal compensatory mechanisms maintain
electrolyte and water metabolism near normal until the late
stages of renal failure. (GFR<10 ml/min).
Sodium : In chronic renal failure maintenance of total
normal body sodium occurs by increased natriuresis per
nephron which may be the result of natriuretic hormone.
However, patients with renal failure have a tendency toward
sodium retention and volume expansion because their
dietary intake exceeds the blunted ability of the diseased
kidney to excrete the usual sodium load.
Patients who have salt losing nephropathy with chronic
renal failure may lose sodium to the point of extracellular
volume contraction and hypotension. These patients require
sufficient dietary sodium to prevent hypotension. The com
mon renal diseases associated with salt wasting are
pyelonephritis, interstitial nephritis, medullary cystic disease
and obstructive nephropathy. When confronted with an
extrarenal cause for increased fluid loss (e.g. vomiting,
diarrhoea, fever), these patients are prone to develop EOF
volume depletion with severe dehydration leading on to
orthostatic hypotension and even vascular collapse. Deple
tion of ECF volume typically results in deterioration of
residual renal function and uremia. Cautious fluid replace
ment may restore intravascular volume, but does not always,
return renal function to previously stable levels.
Potassium : Despite progression of renal failure, most
patients maintain normal serum K+ concentration due to
adaptations in the distal renal tubules and colon, sites where
aldosterone and other factors serve to enhance potassium
secretion.
Oliguria, or disruption
of key adaptive
mechanisms,or antikaliuretic drugs given in CRF patients
will lead to hyperkalemia and its potentially ominous effects
on cardiac function. Acute metabolic acidosis in CRF can
lead to hyperkalemia. Hyperkalemia also occurs in hyporeninemic hypoaldosteronism syndrome which is often seen in
diabetic nephropathy, and chronic interstitial nephritis.
Hypokalemia is uncommon in most cases of CRF. Hypoka
lemia can occur due to excessive diuretic therapy, gastroin
testinal losses, or over zealous restriction of potassium in
diet. Hypokalemia due to primary K+ wasting in urine may
result from Fancori’s syndrome, renal tubular acidosis, or
other forms of hereditary or acquired tubulointerstitial
diseases.
Metabolic acidosis : Metabolic acidosis, which may be
partially compensated by respiratory mechanisms, develops
when exogenous intake and endogenous production of acid
exceeds renal excretory capacity. With progression of renal
disease, ammoniagenesis required for titration of secreted
VOL IV No. 3 & 4-----
St. John's Medical College Journal of Medicine
acid decreases. The extrarenal buffering mechanisms allow
for maintenance of relatively stable, albeit lower than normal
blood bicarbonate concentration. With the recruitment of
various buffer mechanisms and accumulation of organic
acids, there is a progressive rise in the anion gap.
Type IV tubular acidosis, commonly seen in diabetic neph
ropathy and other chronic tubulointerstitial diseases is char
acterised by hyperkalemia, hyperchloraemic acidsosis with a
normal anion gap.
parathyroid gland. In some patients hypercalcaemia may be
seen after significant reductions of serum phosphorus or
after ingestion of large amounts of calcium carbonate.
Mineralization defect in patients on chronic haemodialysis
can lead to hypercalcaemia, which is due to aluminium
deposition in the interface between osteoid and mineralised
bone.10 Hypermagnesemia can occur in CRF therefore,
magnesium containing antacids and cathartics should be
avoided.
Hemotologic abnormalities :
Phosphate, Calcium and Bone : Serum phosphate
concentration begins to rise when GFR falls below 25
percent of normal.7 Retention of phosphate contributes to
hypocalcaemia and increase in plasma PTH levels as seen
in CRF.6
In CRF 1,25 dihydroxy cholecalciferol synthesis is decreased
which leads to hypocalcaemia by decreasing gut reabsorp
tion of calcium and decreasing mobilisation of calcium from
bone. Overproduction of parathyroid hormone, disordered
vitamin D metabolism, chronic metabolic acidosis and
excessive fecal loss of calcium all contribute to renal
osteodytrophy. Renal osteodystrophy encompasses a
number of distinct
skeletal
abnormalities, including
osteomalacia, osteitis fibrosa cystica, osteosclerosis and in
children especially, impaired bone growth.7 Pathogenesis of
renal osteodystrophy in chronic renal failure is shown in
Fig-2.
Renal osteodystrophy is seen more often in growing
children than in adults, and especially in patients with
congenital renal anomalies associated with very slowly
progressive renal insufficiency, and chronic interstitial
nephritis. Clinical symptoms of bone disease occur in less
than 10 percent of predialysis patients with advanced renal
failure, radiologic and histologic abnormalities are seen in
35 and 90 percent respectively.8
Spontaneous fractures are common with renal osteodystro
phy, and are slow to heal. The ribs are most commonly in
volved. Patient may have bone pain, painful joints, proximal
myopathy, gait abnormalities, inability to walk and
extraneous metastatic calcification especially when the
calcium phosphate product is more than 60 percent.8-9
Osteomalacia is secondary to decreased level of 1-25,
dihydroxycholecalciferol, and in few patients it is due to
deposition of aluminium and/or iron at the calcification
front.10 Aluminium level increases with the use of a high
aluminium containing dialysate and taking aluminium
containing phosphate binders, especially in children.
Hyperuricaemia is a common feature of CRF but rarely leads
to symptomatic gout. Hypophosphataemia may occur due to
over zealous administration of phosphate binders. Hypercalcaemia10is rare inpatients with CRF which is because of a
persistent secretion of parathormone from the hyperplastic
Oct - Dec 1991
Normochromic, normocytic anaemia occurs in CRF and
contributes to fatigability and listlessness observed in these
patients. Erythropoiesis is depressed due to decreased
erythropoietin level, iron and folate deficiency, retained
toxins (spermin, spermidine) aluminium intoxication.
Hemolysis also occurs and is because of extra corpuscular
defect since survival of erythrocytes are reduced in CRF.
Hypersplenism also leads to anaemia due to hemolysis.
Acute hemolysis in patients on dialysis can be due to
increased dialysate temperature, exposure to oxidants like
copper, chromium, nitrate present in dialysate and formation
of Anti ‘N’ like antibodies secondary to exposure to formalin.
Gastrointestinal and chronic dialyzer blood loss contributes
to anemia. Abnormal hemostatis is another common
hematologic derangement in CRF characterised by abnormal
bleeding and bruising. Prolongation of bleeding time, de
creased platelet factor III activity, abnormal platelet
aggregation and adhesiveness, impaired prothrombin con
sumption contribute to the clotting defects in uremia.11 In
uremia the levels of Factor VIII coagulant (VIII C) and vWF
activity and concentration are normal but platelet membrane
receptors for vWF binding are modified, which lead to
impaired platelet vessel wall interaction and the bleeding
tendency.12 Increased levels of guanidinosuccimic acids,
inhibits platelet aggregation.
Leucocyte function is impaired in uremia leading to
enhanced suceptibility to infection. Decreased chemotasis,
with resulting impairment of acute inflammatory response
and decreased delayed hypersensitivity occurs in uremia.
Lymphocytopaemia and atrophy of lymphoid structures
occur in CRF. Impaired leucocyte function may also be
because of coexisting factors such as acidosis, hyperglyce
mia, protein calorie malnutrition, and serum and tissue hyper
osmolarity. Mucosal barriers to infection may be defective,
and, in dialysis patients vascular access devices may serve
as common portals *of entry to pathogenic organisms,'
mainly staphylococci. Leucopemia is a common transient
finding in patients exposed tocellophane derived membranes
during dialysis.
Cardiovascular abnormalities :
Arterial hypertension is the most common observed compli
cation of end stage renal disease seen in 80 to 90% of
47 —
St. John’s Medical College Journal of Medicine
Fig 1. Role of sustained increments in glomerular pressure (P)and increased flow (CQA) in the initiation and progression of glomerular sclerosis.
LOSS OFjNEPHRON MASS
1
5
Renal Excretory
function
Renal
Biosynthetic Capacity
i
I w
Jfienal ■
Production
of 1.25(OH)2D3
Retention of
Toxic
Metabolites
i
Hyperphosphatemia
Metabolic
Acidosis
— Hypo
Calcemia
I
4’
I Circulating
*
1,25(OH)2D3
J, Gut
I
*
Absorption
of Calcium
PTH
Secretion
v
,
'
i
I
|
Protein
Calorie
Malnutrition
Responsiveness
of Bone to
1,25(OH)2D3
Dissolution
of Bone
Buffers
Osteomalacia
Bone decalci
fication
Osteoporosis
I
Impaired
Bone Growth
in children
(Renal Rickets)
Calcium
Phosphate
Product
>60
Metastatic
Calcification
I
a
Remodelling
+ Redistribution
of Bone
(Osteosclerosis)
Osteitis
Fibrosa
Fig 2. Pathogenesis of bone diseases in chronic renal failure
48
VOL IV No. 3 & 4 —
St. John’s Medical College Journal of Medicine
patients.13 Major cause of hypertension is fluid overload but
in some it is due to hyperreminemia. A small minority of
these patients develop accelerated or malignant hyperten
sion manifested by markedly elevated systolic, diastolic
pressures, severe hyperreminemia, encephalopathy, seiures, retinopathy, papilledema. In salt losing nephropathy
blood pressure is often normal.
Fluid retention in uremia leads to congestive cardiac failure
and/or pulmonary oedema. In the absence of volume
overload in uremia pulmonary congestion and edema is seen
associated with normal or mildly elevated intracardiac and
pulmonary wedge pressures with increased permeability of
alveolar capillary membranes.
Pericarditis is a common and serious complication of CRF
since its first description by Bright in 1836. This can be
categorized into uremic and dialysis associated.14 Uremic
pericarditis might be attributed to the biochemical alteration
seen in uremia as evidenced by its rapid response to dialytic
therapy in most patients. Incidence of uremic pericarditis is
decreased to 6 to 17 percent due to early initiation of
dialytic therapy and improved conservative manage
ment. 1415 Pericarditis occurs in 8 to 17 percent of patients who
have been stablized on maintenance dialysis.16 This may
be due to inadequate dialysis, hyperparathyroidism,
heparin therapy, infection, fluid overload and an immunol
ogic mechanism. Systemic symptoms such as chest pain
and fever, hemodynamic compromise and tamponade are
more frequent in dialysis associated pericarditis than in
uremic pericarditis.14 Fluid of most dialysis associated peri
carditis is serosanguineous to bloody and the fluid of uremic
pericarditis is usually serous or sero fibrinous.14
Chronically dialyzed patients have a high incidence of
accelerated atherosclerosis, leading to development of
significant coronary, cerebral and peripheral vascular dis
ease.17 These complications are due to long term
hypertension, hyperlipidemia, glucose intolerance, and me
tastatic vascular and myocardial calcification.
Neuromuscular abnormalities :
Central nervous system dysfunction including inability to
concentrate, drowsiness, and insomnia are among the
earliest symptom of uraemia. Stupor, seizures, and coma
are common in terminal uremia. This whole symptom
complex is thought to be due to increased parathormone
leading to increased intracellular calcium in brain.18
Peripheral neuropathy is a relatively common complication of
CRF. Initially sensory nerve involvement exceeds motor,
lower extremities are involved more than upper, and the distal
portions of the extremeties more than the proximal. The
‘Testless legs syndrome", characterized by ill defined sensa
tions of discomfort in the legs and frequent leg movements
are disturbing symptom in some uremic patient. If dialysis
Oct Dec 1991
is not instituted now, motor involvement occurs often leading
to loss of deep tenden reflexes, weakness, peroneal nerve
palsy and eventually flaccid quadriplegia.
Two types of neurologic disturbances appear to be unique
to patients on chronic dialysis. Dialysis dementia, seen in
patients on long term hemodialysis, is characterised by
speech dyspraxia, myoclonus, dementia and eventually
seizures and death. Aluminum intoxication is one of the
possible causative factors. Dialysis disequilibrium syndrome,
occurs during the first few dialysis, in association with rapid
reduction of blood urea levels. Nause, vomiting, headache,
muscle twitching, blurring
of
vision disorientation,
drowsiness and seizures have been attributed to more rapid
change in pH and reduction in osmolaity of extracellular
than intracellular fluids leading to cerebral oedema and
raised intracranial pressure19.
Gastro intestinal abnormalities : Anorexia, hiccups,
nausea, vomiting are common and early manifestation of
uremia. Uremic fetor, a uriniferous odor to the breath,
derives from the breakdown of urea in saliva to ammonia and
is often associated with unpleasant taste sensation.
Mucosal ulceration leading to blood loss can occur at any
level of gastro intestinal tract. Peptic ulcer disease is
common which can be related to increased gastric acidity,
hypersecretion of gastric or secondary hyperparathy
roidism. Hepatic disease is seen in patients on long term
haemodialysis. 33 percent of hemodialysis patients were
found to have liver dysfunction.20 With screening of blood
for HBsAg, before trans-fusing the incidence of HBsAg
positivity on dialysis has reduced considerably. HBsAg
positive chronic hemo-dialysis patients.
Persistant ascitic fluid accumulation in patients on chronic
haemodialysis may be due to liver disease, cardiac cause,
peritonitis-tubercular, fungal or bacterial, protein loss or
starvation. The term dialysis ascites denotes persistant
ascites in chronic haemodialysis patients in the absence of
above mentioned causes. It is a serious sign of failure of
haemodialysis regimen often accompanied by anorexia,
muscle wasting and worsening neuropathy. Improvement
is rarely induced by intraperitoneal instillation of steroids,
albumin infusion
or intensive ultrafilteration during
dialysis.22
Endocrine Metabolic disturbances :
Hypothermia is aknownfeatureof uremia. It is indicative of
thermo regulatory failure which is probably due to wide
spread inhibition of Na, K+ ATPase by uremic toxins and
circulating inhibitor factor of cycloxygenase pathway.23
Impaired glucose tolerance (azotemic pseudo diabetes) in
uremia is due to diminished sensitivity to action of insulin on
its target tissues.24 Other possible factors contributing to
glucose, intolerance include intracellular deficits of
49 —
St. John’s Medical College Journal of Medicine
potassium, metabolic acidosis, increased levels of
glucagon and other hormones including catecholamines,
growth hormone and prolactin as well as the myriad of
potentially toxic metabolites retained in ORF. Decreased
catabolism of insulin may lead to decreased or no require
ment of insulin in diabeties with CRF. Repeated episodes
of hypoglycaemia may focus attention on deterioration of
renal function in the insulin treated diabetic patient25.
Hypertriglyceridemia and decreased high density lipopro
tein cholesterol are common in uremia. Hypertriglyceridemia
may be due to lipogenic effect of hyper insulinism and
decreased rate of removal of triglycerides due to depressed
activity of lipoprotein lipase in uremia. The high incidence of
premature atherosclerosis in patients on chronic dialysis
may be attributed to abnormalities in lipid metabolism.
There is abnormalities in circulating thyroxine, growth
hormone, aldosterone and cortisol levels. Growth retardation
in uremia occurs inspite of increased growth hormone level
and one of the factors may be abnormal action of somato
medins.26
Secondary hyper-parathyroidism occurs in uremia and
over secretion of this hormone is potentially responsible
for widespread tissue dysfunction in uremia.27
2.
Pallor, Hyperpigmentation, ecchymoses, excoria
tions, uremic frost, Hypertension, Cardiomegaly,
Haemic murmur, Pericardial rub, edema, signs of
pericardial effusion and Cardiac tamponade.
Signs of peripheral neuropathy and higher func
tion abnormalities, proximal myopathy Growth re
tardation, pathological fractures, bone tender
ness, arthritis, extraosseous calcifications Retino
pathy - hypertensive and/or diabetic. Palpable
Kidneys - Polycystic kidneys, obstructive uropathy
3.
4.
The skin shows many abnormalities, pallor, ecchymoses
and hematomas, excoriations, pruritus, and general
cutaneous consequences of protein calorie malnutrition. In
advanced uremia, urea concentrations in sweat may reach
sufficiently high levels that after evaporation a fine white
powder can be found on the skin surface, the so called uremic
frost. Hemochromatosis causes a slate gray bronze
discolouration of the skin and is commonly seen in patients
received multiple transfusions on dialysis.
5.
Management
I.
50
Renal Biopsy
Indicated in patients With normal or large size
kidneys with raised blood urea and creatinine to
find the treatable cause. The treatable paren
chymal disease ate Lupus nephritis, Renal
Vasculitis like Polyarteritis nodosa
and
Wegener’s Granulomatosis, and Malignant hyper
tensive nephropathy.
History
History of oliguria, polyuria, nocturia, haematuria. History of recurrent urinary tract infec
tion. Symptoms of bladder dysfunction, Uremic
symptoms. History of systemic diseases like
Diabetes mellitus, Hypertension. History of
exposure to toxins or drugs. Family history of renal
disease - polycystic kidney disease, Alport’s
syndrome.
Radiological findings
Chest X-Ray Pulmonary Oedema, Cardiomegaly,
Pericardial effusion or pleural effusion Plain X Ray
KUB - Radio opaguq stones, renal contour and
size Ultrasonography - usually bilaterally small
contracted kidneys with increased cortical echo
genecity. Normal size kidneys with chronic renal
failure is seen in diabetic nephropathy, amy
loidosis polycystic kidney disease, scleroderma
or malignant hypertension. Obstructive nephropa
thy will reveal bilateral dilatation of pevicalyceal
system with decrease in parenchymal thickness.
X-rays of hands and feet to look for deminerali
zation
subperiosteal reabsorption or vascular
calcification Bone densitometry for Osteopenia
or Osteosclerosis type of renal Osteodystrophy.
Nerve conduction studies for assessment of
peripheral neuropathy,
Dermatologic abnormalities :
1.
Laboratory findings :
Azotaemia - raised Blood urea and creatinine Hy
perkalemia, hyponatremia, Hyperphosphatemia,
hypocalcaemia and increased alkaline phospha
tase indicate renal osteodystrophy Metabolic aci
dosis Anemia usually normocytic normochronic
type. Proteinuria-nephrotic range seen in diabetic
nephropathy,
reflux nephropathy, amyloidosis
and focal glomerular sclerosis. Broad waxy casts,
Hematuria may be present.
In men with CRF, including those on dialysis, impotence,
oligospermia and germinal cell dysplasia are common as
are reduced plasma testerone levels.28 In women, oestrogen
levels are low, and amenorrhoea and repeated abortions
are early manifestations of uremia.29
Diagnostic approach to patients with chronic
renal failure
Physical examination :
Conservative management of patients with
VOL IV No. 3 & 4-----
St. John's Medical College Journal of Medicine
chronic renal failure :
A.
Measures to prevent aggravating factors leading to
renal failure:
1.
Avoid volume depletion and hypotension by avoiding ex
cessive use of diuretics, antihypertensive medications, or
severe restriction of dietary sodium. Prompt diagnosis
and appropriate therapy for vomiting and diarrhoea.
2.
Aminoglycosides, Vancomycin, Cimetidine, Clofibrate,
Antiarrhythmic drugs, Cytotoxic drugs and various antibi
otics dosages should be reduced according to creatinine
clearance tests and drug levels should be monitored.
3.
Drugs which are contraindicated in Chronic renal failure
are nitrofurantoin, spironolactone, triamterene, amiloride, phenformin. sulphonylureas and cephaloridine and
non steroid antiinflammatory agents.
4.
Control of systemic infection and urinary infection with
appropriate antibiotics in appropiratedosage corrected to
creatinine clearance.
5.
Relief of obstruction if present.
B. Diet : Data from animal studies have shown that a low
protein diet can slow the progression of disease as increased
protein in diet leads to increased renal blood flow and GFR
leading to glomerulo sclerosis30. The protein restriction
lowers the dietary acid load, thereby reducing ammonia
production of the remnant nephron which could diminish
complement activation and its inflammatory and cytotoxic
consequences. This will also reduce the production of urea
thus reducing the symptoms such as nause, vomiting,
drowsiness. The protein intake should be reduced to
0.6 gms/kg/day of which at least 0.35 gm/kg/day is of high
biologic value protein to ensure sufficient intake of essential
amino acids.31 Patients may be supplemented with essential
amino acid or ketoacid mixture of about 10 to 20 gm/ day
with protein 0.28 gm/kg/day.32 Patient on hemodialysis or
continuous ambulatory peritoneal dialysis protein intake is
liberalised to 1 to 1.5 gm/kg/day. This should be accompanied
by adequate calorie intake (35 to 50 KCal/kg/day) to prevent
protein catabolism. Potassium should be restricted to 40 to
60 meq/day. Potassium rich food substances should be
avoided such as fruit juices, coconut water, citrous fruits and
dry fruits. Magnesium containing substances should be
avoided as hypermangnesemia can occur in renal insuffi
ciency. Low phosphate diet is also recommend upto 0.6 to
0.8 gm/day especially beneficial in renal osteodystrophy.
Salt and fluid restriction is determined on individual basis,
influenced by cardiovascular status and by GFR. In presence
of oedema, oliguria, dilutional hyponatremia fluid and salt
restriction is advocated. Daily weight recording is essential
according to which salt and fluid intake can be determined.
Oct - Dec 1991
C. Control of hypertension may slow the progression of
renal insufficiency which is particularly important in patients
with malignant hypertension. The use of angiotension
coverting enzyme inhibitors is said to be especially helpful
in diabetic nephropathy by reducing glomerular hyperten
sion injury. In most cases routine anti hypertensive drug
therapy is effective. In some cases, salt and fluid restriction
with ultrafilteration or initiation of dialysis will control
hypertension.
D. Acidosis should be treated when serum bicarbonate falls
to less than 16 meq/litre or when symptoms are present.
Sodabicarbonate is administered in a dose of 3 gms to 6 gms/
day. In presence of severe acidosis haemodialysis or
peritoneal dialysis is indicated. Salt restriction in diet is
essential when soda bicarbonate is given for treatment of
acidosis.
E. Hyperkalemia if it occurs due to some aggravating factor
such as tissue breakdown, transient worsening of acidosis
or antikaliuretic drug ingestion then the therapy should be
directed to correct the source of hyperkalemia. In CRF
patients serum potassium upto 6 meq/litre is well tolerated.
If potassium increases above this then it should be treated
immediately by 10 ml 10% Calcium gluconate IV for 1 to 5
minutes.
Glucose insulin drip (30% Dextrose 500 ml with 30 units
insulin, at the rate of 100 ml in first hourthen 20ml/hr) or OV
soda bicarbonate which will reduce potassium level in 30
minutes by causing intracellular shift of potassium.
Cation exchange resin kayexalate given orally 20 to 30 gms
three to four times daily can bring down serum potassium
level. It takes 1 to 2 hour to show its effect. It can be given in
the form of retention enema along with 100 to 200 ml of
50 to 70% sorbitol. Serum potassium of more than 7 meq/
litre, dialysis is indicated.
F. Anemia can be treated with recombinant erythropoietin in
a dose of 50 to 100 units/kg twice or thrice a week so
haemoglobin level is maintained around 9 to 10 gm%.33
Serum iron and serum ferritin level should be estimated and
accordingly oral iron supplementation should be given.
Patient should be treated with folic acid and vitamin B12 for
deficiency of these vitamins, or desferoxamine for anemia
due to aluminum excess.34 Blood transfusion are given in
patients on dialysis who are symptomatic due to severe
anemia but hyper transfusion itself can lead to anemia due
to bone marrow depression.
G. Hyperphosphataemia is treated with phosphate binder
Aluminum hydroxide with meals (30 ml Q8h) or Calcium
Carbonate (1gm 8 hrly) with meals. Doses should be titrated
to maintain serum phosphate level. Calcium is supple
mented to maintain serum calcium levels. Calcium taken
with meals binds dietary phosphates and is poorly absorbed
51
St. John’s Medical College Journal of Medicine
but when taken between meals, is more efficiently absorbed
and is more effective in treatment for hypocalcemia.
H. Bone disease of uremia is treated by phosphate binders
to reduce phorphorus level, oral calcium supplementation,
and active Vitamin D3 1,25 dihydroxycholecalciferol
(Rocaltrol) 0.25 ug to lug/day.35 Intravenous calciol injection
reduces serum parathomone level36. Aluminium related
bone disease, osteomalacia, is treated with desferoxamine,
which chelates the aluminum37.
Indications for parathyroidectomy in CRF
Unsuccessful medical treatment for
secondary
hyperparathyroidism.
2. Infractable pruritus not responding to medical treatment
or dialysis.
3. Severe and progressive skeletal pain or fractures
4. Persistant symptomatic hypercalcemia
1.
I. Pericarditis in renal failure is treated first with intensive
dialysis in hemodynamically stable patient and systemic
anticoagulation is avoided to minimize the possible occur
rence of hemorrhagic tamponade. Resolution of dialysis
associated pericarditis with intensified dialysis has been
reported to occur in 55 percent of patietns38. Enlarging
pericardial effusion or persistent effusion after 10 to 14 days
of intensive dialysis therapy warrants for immediate
pericardiocentesis and if necessary with catheter drainage
and/or local instillation of steroids. If still does not resolve
then pericardiectomy is indicated. In haemodynamically
unstable patients or with cardiac tamponade pericardiocen
tesis is first indicated followed by, if necessary pericar
diectomy.
J. Abnormal hemostasis in CRF can be corrected with
peritoneal dialysis
(removal of middle molecules),
injecting cryoprecipitate, Desmopression, blood transfusion
or conjugated oestrogen.391404’ This treatment is indicated
when patient is subjected for surgery or any biopsy
procedures to prevent bleeding.
K. Pruritus can be treated by strict control of serum phos
phate with phosphate binders and low phosphate diet. Mois
turizing skin cream is used for dry skin. Diphenhydramine, 10
to 25 mg orally twice to thrice daily is sometimes helpful.
While conservative measures are being carried out, it is
necessary to explain the prognosis and the other modalities
of treatment for end stage renal disease i.e. dialysis and
transplantation. The more knowledgiable the patients are,
the earlier and more appropriate will be their decision at a
later time. Dialysis and transplant therapy Is instituted
when conservative therapy Is not sufficient to keep patient
with renal failure symptom free or patient is too ill to be
maintained comfortably with the usual methods of treatment.
Haemodialysis employs the process of diffusion across a
52
semi permeable membrane to remove unwanted substances
from the blood while adding desirable component43. Indica
tions for initiation of dialysis are listed below.
Indications for Initiation of Dialysis in CRF
Pulmonary Oedema - Ultrafilteration + Dialysis
Hyperkalemia and other electrolyte abnormalities
Severe metabolic acidosis
Uremic encephalopathy, neuropathy
Uremic pericarditis
Uremic bleeding
Persistent nausea, Vomiting, weakness
Blood Urea > 250 mg/dl and S.Creatinine > 10 mg/dl
Haemodialysis is done two to three times a week and each
time for four to five hours totalling 10 to 15 hours of dialysis per
week. In patients with hyper catabolism or complicating
severe illness the dialysis is performed daily for short
duration in each sitting. The time depends upon body size,
residual
renal function, dietary intake, complicating ill
nesses, the degree of anabolism or catabolism.
TABLE 3: Complications of Haemodialysis
Vascular access infection, thrombosis and aneurysm
Hypotension
Hypoxia
Cramps
Pyrogenic reactions
First use syndrome - restlessness, backpain, chest
pain, bronchospasm, hypoxia, hypotension, pruritus,
leukopenia, tremors headache and rarely anaphylaxis.
7. Complications from blood transfusion - Transfusion re
action, sensitisation to Cytomegalovirus, human im
muno deficiency virus, hepatitis B or Non A Non B and
HLA antigens.
8. Latrogenic complications - air embolism, improper dialy
sate leading to hemolysis and hypo or hypernatremia^,
over heated dialysis Insufficient or excessive use of anti
coagulants.
9. Dialysis associated ascites or pericarditis
10. Dialysis associated ascites or pericarditis
11. Dialysis disequilibrium syndrome
12. Dialysis dementia
13. Osteomalacia - Aluminium intoxication or malnutrition
Vitamin 0 deficiency
14. Amyloidosis - Carpel tunnel, syndrome, arthropathy,
bone cysts
15. Acquired renal cysts * Benign or malignant
15. Septicaemia
1.
2.
3.
4.
5.
6.
This is more efficient than peritoneal dialysis allowing rapid
changes in serum values. Haemodialysis can be performed
at home but patient requires an assistant at home.
Peritoneal dialysis, like haemodialysis may be performed
in various settings and with a number of different techVOL IV No. 3 & 4 —
St. John's Medical College Journal of Medicine
mques.43 Chronic
peritoneal
dialysis has become
successful after development of a permanent peritoneal
cathetar in 1968- TheTenckhoff catheter. The peritoneum
acts as a membrance separating blood in capillaries from
peritoneal dialysis fluid. The peritoneal dialysis is performed
constantly for 24 to 48 hrs with one litre exchange per hour
in a hospital setting. The other techniques are intermittent
peritoneal dialysis (IPD) continuous ambulatory peritoneal
dialysis (CAPO) and continuous cyclic peritoneal dialysis
(CPD). Advantages of peritoneal dialysis are avoidance of
heparinization and vascular surgery and a slower clearence
rate which may be advantageous in some patients with
cardio vascular instability. It is more amenable to self
treatment. Disadvantages include the longer treatment
time, either longer periods intermittently or continuous in
volvement. Contraindicated in patients with recent abdomi
nal surgery or pulmonary compromise. Complications are
exit wound infection, catheter tunnel infection, peritonitis,
cuff extrusion, leakage from the side of the catheter, hyper
triglyceridemia, hyper cholestrolemia, obesity, moderate
protein loss, inguinal and abdominal hernias.
Mortality and morbidity of patients on long term dialysis
increases with age and is significantly higher in patients with
diabetes mellitus or hypertension as a cause of renal failure.
First year mortality is more (14.2 to 15.2 percent) than in
consecutive years irrespective of age. Approximately 10 to
20 percent of patients with end stage renal disease are
totally rehabilitated by dialysis, and another 30 to 40 percent
of non diabetic patients may be expected to be rehabilitated
to a functional status even if not employed. Diabetics have
a rehabilitation and survival rate lower than non diabetic
patients on dialysis.
Kidney transplantation has allowed remarkable rehabilitation
of patients with end stage renal disease and is an established
mode of treatment for this disorder. The observed 5 year
patient survival was reported to be better with transplantation
(living related donor, 90 percent) than with dialysis (85 per
cent) which is same with cadaver doner renal transplan
tation. Contraindication to renal transplantation are listed in
Table 4.
TABLE 4: Contraindications to kidney transplantation
Uncontrolled Psychosis
Ongoing substance abuse
Medical noncompliance
Age>60 Yrs (Varies among centres)
Active infection
Malignancy 2 -4 yrs after curative resection
Metabolic bone disease - Severe secondary hyperpara
thyroidism
Active peptic ulcer disease
Cardio Vascular disease - Severe left ventricular dysfunction
and severe coronary artery disease
Urologic abnormalities - Severe reflux or neurogenic bladder
Oct - Dec 1991
Systemic illness - Fabry’s disease, primary hyperoxalosis.
Kidneys for transplantation are obtained from living or
cadaver donors. One year graft survival rate is increased to
90 percent with patient survival of 95 percent in living
related donor transplantation.44 In cadaver transplantation
or unmatched kidney transplantation the graft survival rate
at the end of 1 year is 77 percent with patient survival rate of
85 percent. This increase is due to Cyclosporine. The quality
of life improves after renal transplantation, especially
children with chronic renal failure as with the advent of
cyclosporine, steroid may be omitted from immunosuppres
sive regimen to prevent growth retardation.
CONCLUSION
Chronic renal failure is due to slow, progressive deterioration
of renal function. This should be diagnosed at earlier stage.
The progression of renal disease can be prevented by
diet restriction, control of hypertension and diabetes,
avoiding nephrotoxic drugs and early detection and
treatment of aggravating factors. Patients with chronic
renal failure should be explained about the treatment
modalities, dialysis and renal transplantation and the cost of
each treatment so that they are well prepared and can take
appropriate decision when required. Renal transplantation
does represent one of the miracles of modern medicine
when one considers the dramatic improvements that have
occured in the outcome of renal transplantation over the
past 25 years. Since the higher risk patients are being
transplanted and patients are surviving many years after
transplantation, more attention should be given to the risk
factors that influence patient survival
particularly risk
factors for cardio-vascular disease.
With the advent of cyclosporine the graft and patient
survival has improved significantly. Children can undergo
transplantation without using steroids as immunosuppres
sive which can lead to growth retardation.
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27. Massry SG. The toxic effects of parathyroid hormone in uremia.
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14. Ogburn HM, Ayrus JC and Eknoyan G, Pericarditis in renal failure.
Therapeutic considerations Dial. Transplant 1978;7:1133.
15. Comty CM, Wathen R and Shapiro Fl Pericarditis in chronic uremia and
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16. Luff FD, Gilman JK and Weman AE. Pericarditis in the patient with
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1973:4:1777.
20. Tbussaint C, Dupont E, Vanherwaghem JL et al. Liver disease in
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Gastroienterol 1982:77:73.
DA.
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Ann
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1980:18:92.
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38. De Pace NL, Nesteco PF, Schwartz Ab et al : Predicting success of
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39. Janson PA, Jubliere SJ. Weinstein MJ and Deykin D : Treatment of the
bleeding tendency in uremia with
cryoprecipitate.
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J
23. Tanaka H, Uminoto K, Izuni N et al. Platelet cyclo-oxygenase (PCO) in
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24. Smith D, and De Fronzo RA. Insulin resistance in uremia mediated by
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25. Strauss RG, Argy WP Jr., and Schreiner GE, Diabetic glomerulo
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32. Barsotti G, Guiducci A, Ciardella F and Giovannetti s : Effects on renal
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40. Manucci PM, Remuzzi K, Pusineri F et al : Deamino-8-d-arginina
Vasopressin shortens the bleeding time in uremia. N Engl J Med 1983:308:8,
41. Lindsay RM Friesen M. Koens F et al: Platelet function in patients Oh
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42. Hakim RM and Lazarus JM : Medical aspects of hemodialysis in the
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ed, Philadelphia^ Saunders 1988;
VOL IV No. 3 & 4-----
NEPHROLOGY SYMPOSIUM
St. John's Medical College Journal of Medicine
URINARY TRACT INFECTION IN CHILDREN
V.J.JOSEPH, M.YESHWANTH
Infection of the urinary tract (UTI) is etipathologically and
symptomatically different in children from that of adults.
Every child regardless of sex or age requires a detailed
workup at the first episode of infection.
EPIDEMIOLOGY
Among children who tend to develop UTI, 2/3rd of them do so
in the first 3 months of life1 and males develop it earlier
than females, especially during the neonatal period, one
percent of boys and 3% of girls experience UTI before 11
years of age and 1.4/1000 neonates develop UTI with a re
currence risk of 25%. Male neonates are affected 2.5 times
more than females and there is no difference among prema
ture or mature neonates. Between 1.7 and 4.1% of febrile
children have .UTI as the underlying cause.
ETIOPATHOGENESIS
Factors like bladder neck obstruction, distal urethral stenosis,
hematogenous infection (except in neonatal period) fecal
soiling, short female urethra and social conditions which were
considered causative factors in childhood UTI, are no
longer considered significant.
6.
K, and K5
Protection against immune
system
7. Various secreted
enzymes
Neutralize host defence
eg. IgA
TABLE 2 : Host Factors - protecting or
predisposing?
SITE
Colon colonization
SUGGESTED ROLE
Urethral ascent
2. Serum resistance factor Protects against normal killing
action of serum
3. Colicin V
Iron sequestration
4. Novel outer membrane
proteins
Virulence marker or protection
against alternative pathway of
complement lysis
Kidney colonization
Inflammation
DR. V. J. JOSEPH
DR. M. YESHWANTH
DEPARTMENT OF PAEDIATRICS
ST.JOHN'S MEDICAL COLLEGE AND HOSPITAL
BANGALORE - 560 034.
__ imityJl
Oct-Dec 1991
--------------
326» V Main
FACTOR
1.
2.
1.
2.
Vaginal and periurethral 1.
Colonization
2.
Urine growth and
bladder emptying
Iron sequestration
1. Hemolysins
Prevent direct association
with phagocytes
Bladder antibacterial
defence mechanism
I : BACTERIAL VIRULENCE FACTORS
VIRULENCE FACTOR
O group 2,4,6,8,
18 ab, 75
Bladder migration
The bacterium as it migrates, has to traverse an array of host
defence mechanisms to invade, colonize, grow and survive
in the new environment of kidney. These include bacterial
factors and host factors that determine pathogenesis of UTI
in children, which is summarised in Table 1 & 2.
TABLE
5.
Ecologic competition
Antimicrobial therapy
Poor hygiene
Age-high risk for neonatal UTI
Cell adhesion-possible
increase in receptor density
Competition with other vaginal
flora
3. IgA antibody
4. Vaginal pH
1. Short female urethra
2. Retrograde urine flow
1. Mucous
2. SlgA antibody-local decrease
in production leads to bacterial
colonization
3. Cell adhesion-possible
increase in receptor density
1. pH
2. Urine osmolality
3. Voiding patterns
4. Residual Urine
1. Reflux
2. Brownian movement of
ureteral urine
3. Endotoxin mediated a
peristalsis/hypoperistalsis
1. Cell adhesion-possible
increase in receptor density
2. K and 0 antigens of E.coli
3. Serum resistance
1. Local solute concentration
2. Blood supply
3. Inpaired leucocyte activity
4. Variable antibody production
against 0 but not K.
The majority of uropathogens are of the enterobacteriaceae
$E^lch
accounts for 75% of infection. Other
J Slock------- ------------------------------------ 55 —
Korameng^la
Bangalore-560034
St. John’s Medical College Journal of Medicine
organisms encountered are Klebsiella, Proteins, Enterobacter and rarely Pseudomonas and Staphylococcus
saprophyticus.
by clean catch midstream specimen or any growth obtained
by suprapubic aspiration (SPA) is considered as diagnostic
of UTI.
The host defence mechanisms that favour or protect against
UTI varies in each age group and different sexes. The
accepted observations in children are :
In neonates and infants the most preferred method of urine
collection is SPA. It is also indicated in persistant bacteriuria
of doubtful significance, obstruction of out flow tract or very
seriously ill patients3 Adhesive plastic bag collection is an
acceptable alternative method of collection in infants. The
sample should be forwarded for evaluation within 15-20
minutes of collection. Catheterization for collection of urine
just for culture is condemned.
1. UTI in male children is predominantly a disease of neo
nates and infants.
2. Periurethral colonization varies with age :
- dense colonization occurs in newborn boys, which is
absent in girls who develop colonization by 2nd week or
later.
3. Most children outgrow their propensity for UTI as they
grow older.
4. A proportion of girls are UTI prone and they have dense
introital colonization with Gramnegative bacteria. These
children are shown to have buccal mucosa and uro
genital epithelium which has increased adherence for
bacteria.
5. First time UTI is unusual in males over one year.
Once infection is established, the antibodies produced
may be directed against renal cells and Tam-Horfall
protein, resulting in renal scaring.
Clinical features
The symptomatology of UTI varies with age. In neonates
it simulates neonatal sepsis, and CNS symptoms occur in
28%. Older infants present with nonspecific sytemic symp
toms but are not as ill as neonates. Symptoms include fever,
lethargy, decreased appetite, poor weight gain, vomiting
and diarrhoea, abdominal pain, frequency and dribbling,
poor stream and malodorus urine. The classical features of
poor stream and distended bladder should arouse one’s
suspicion of posterior urethral valves. Unusual somnolence
may result from hyperammonemia caused by infection with
a urea splitting organism like proteus. The classical signs and
symptoms of UTI like fever, dysuria, enuresis, flank pain and
renal angle tenderness occur in older children. About 1.74.1 % of febrile children below 5 years have UTI as the cause.
Associated anomalies in physical examination may signal
structural problems in the urinary tract. These include
preauricularpits, cardiac defects, abdominal muscle defect,
cryptorchidism, hypospadias, and skeletal deformities.
CLASSIFICATION
UTI was formerly classified as complicated and uncompli
cated on the basis of age, systemic symptoms, physical and
lab. findings and presence of underlying urinary abnormali
ties. This classification is not well accepted now, as un
complicated. UTI in this corresponds to covert bacteriuria.
The most important factor regarding urine examination apart
from proper collection is transportation. After 24 hrs at
room temperature most urine specimens will have similar
numbers of bacteria irrespective of the number present ai
voiding. At0-4°C.the bacterial count remains unchanged
for 48 hrs. Hence the samples are to be forwarded within
15 minutes of collection or stored at 0-4° for a maximum of
48 hrs.
Antibiotics should be stopped for > 72 hrs prior to collection
and no antiseptics used to wash the perineum. On
microscopic examination presence of 1 rod/HPF corre
sponds to 10,000-100,000 bacteria per ml. Demonstration of
pyuria indicates inflammation of the renal collecting system
which could be of nonbacterial or bacterial origin. More than
10 WBC/HPF is seen in about 80% of children with
symptomatic UTI4.
Demonstration of WBC esterase in urine, and urinary nitrate
detection, are used as other methods of demonstration
of secondary phenomena of infection.
Though there are various methods like Fairley Washout
technique described for localization of infection., it has no
relevance to practical management.
Assesment of renal function is necessary in all children with
UTI. Persistance of reduction in renal concentrating capacity
formore than 12 weeks or elevated BU or creatinine (except
in newborn period) suggest obstruction, renal scarring or
persistant infection.
RADIOLOGICAL EVALUATION
All pediatric patients with well documented UTI should
undergo Urologic evaluation9 The main objectives of evalu
ation are
1. To detect factors that render kidney susceptible to
parenchymal damage like underlying structural anoma
lies.
LAB DIAGNOSIS
2.
To detect parenchymal destruction if present.
A growth of >105 colonies of bacteria per ml of urine obtained
3.
To check the rate of growth of the kidney.
56
VOL IV No. 3 & 4-----
St. John’s Medical College Journal of Medicine
IMAGING TECHNIQUES
KUB may reveal renal calculi, absent psoas shadow or
abnormal renal contour suggestive of renal inflammation
which is better demonstrated in a tomogram.
RENAL ULTRASOUND (U.S)
UltraSound has superseded Intravenous Urography (IVU) as
the first mode of investigation in patients with UTI. It can noninvasively assess the renal paranchymal thickness,
scarring, hydronephrosis, pyonephrosis or perinephric ab
scess. It can also suggest an obstructive pathology like
PUV. The disadvantage is that the study is dependant on the
interpretive and performance skill of the radiologist.
IVU
Except for its invasive nature IVU is better in delineating the
collecting system.
Since preservation of renal tissue in the aim of the therapeutic
efforts, the growth of the kidney needs to be assessed
periodically. The revaluation is to be done after 6 months
when infection has occured in the first year of life and after
2 months if infection has occured in the second year of life.
When the onset occurs later the checkup is done after an
interval of 2 years or more
RADIO NUCLEIDE SCANS
99MTC Dimercapto Susinic acid (DMSA) Scan has replaced
the other radioneuclide studies for evaluation of UTI.
Formerly Gallium 67 I31 hippuran, Technitium"glucohepatonate scans were used. Since the contrast medium for IVU
is handled by kidney as a pure glomerular filtrate the image
by IVU reflects only filtration and can demonstrate both the
cortex and the collecting system. DMSA is fixed in the
proximal tubule and in the loop of Henle. Thus the image
reflected is the functioning renal tubular mass. Thus IVU is
recommended for the study of calyceal collecting system
anomalies and also for demonstrating global thinning of
kidneys. DMSA is the best method for studying focal renal
scarring and to detect presence of functional renal tissue
when nephrectomy is considered6 7 99MTC DTPA Scan is
used for assessing renal function.
IMMUNOLOGIC METHODS
Though various methods like agglutination tests and detec
tion of fluorescent antibody coated bacteria are available, its
use is limited in children. Estimation of urinary secretory IgA
(SlgA) expressed as a ratio of creatinine is recently reported
and low level of SlgA is considered as a specific marker for
UTI8
NATURAL HISTORY
Recurrent bacteriuria ceases as the child grows older. 20%
cure rate is expected after each successful treatment of
UTI9-10-1’ The severity of renal damage producing UTI de
Oct - Dec 1991
pends on presence of underlying renal abnormalities and the
nature of it.
COVERT BACTERIURIA
The outcome of covert bacteriuria and its management are
less controversial now. The current consensus are that these
patients do not require treatment regardless of the type and
nature of the underlying pathology12.
For renal scarring to occur among the symptomatic
bacteriuric children, there should be recurrent UTI or pres
ence of underlying abnormalities.
The incidence of
underlying urinary tract abnormalities in children with
symptomatic UTI is 50% among western population.
Information available from South India indicates that the
incidence is as high as 85%. The main pathology isvesico
ureteric reflux (VUR) accounting for 35-40% of all case of
UTI.13 In Indian studies PUV is the commonest lesion but this
apparent high incidence could be because only the seriously
affected children with UTI go for complete evaluation in our
country.14
About 20% patients with UTI develop renal scarring and it
takes about 18-24 months for radiological appearance. There
are certain types of renal papillae that permit intrarenal reflux
and these papillae subtend their site for paranchymal
scarring when UTI occurs.
In children with VUR, the renal growth is normal, if they do not
develop UTI. Growth is impaired in the presence of scarring
or infection, both of which are transient. In severe VUR
the prognosis for renal growth is poor. As child grows the
unilateral scarring is well compensated by hypertrophy of the
contralateral normal kidney. In such cases the prognosis may
not be influenced by age of onset, sex, reflux or number of
infection and the GFR and mean renal mass may remain 9899% normal.
COMPLICATIONS
Complications of renal scarring include loss of renal
concentrating capacity, inability to acidify urine, proteinuria,
hypertension, azotemia, and renal failure. The incidence of
hypertension in unilateral scarring is less (10%) compared
to bilateral scarring (18%). Level of plasma renin activity
(PRA) may predict the propensity to develop hypertension in
chronic renal scarring. In a high percentage of patients with
VUR progressive renal failure occurs inspite of surgical
treatment and role of surgery even in grade IV & V VUR
is currently controversial9.
RECURRENCE
The risk for recurrence of UTI is 3 times greater in girls at any
age than in boys except in the neonates. The risk of further
infection in a patient who already had UTI is many times
57 —
St. John’s Medical College Journal of Medicine
greater (67%) than the risk of primary infection in healthy
controls (2,8%),15
circumcision has revised previous report to deleniate the
potential medical benefits of neonatal circumcision.16
MANAGEMENT
All patients with complicated UTI would require a close follow
up. The ideal followup would be 1 st visit after 2-3 days of
discharge and after 3 weeks then once in 4 months for a
minimum of 1 year.
Management of UTI includes the accurate diagnosis at the
earliest of the 1st symptomatic infection, proper antimicrobial
therapy, evaluation of underlying risk factors, regular
followup and discussion with parents on the magnitude of
the problem, its consequences, and future problems that
may arise in due course.
In general, children without fever and only frequency and
foul smelling urine have no significant risks. These groups
would require about
3-5 days of antibiotics and a urine
culture within 1 week to show that the urine is sterile.4
Regular followup to watch for complications is recom
mended.
The children with complicated UTI require speedy diagnosis
and early treatment. Immediate therapy has beneficial effect
on the prevention of renal damage. Parenteral therapy with
a synthetic pencilJin and aminoglycoside need to be initiated
till cultures are ready. The appropriate antibiotics are then to
be continued for 2 weeks. If the blood culture is negative,
3 to 5 days parenteral therapy followed by oral medication
for 5-7 days would suffice. However, the duration of
therapy is Still controversial with some authors recommend
ing treatment for 1 -2 months, which would be preferable in
patients with grade IV or V reflux.2
Renal & bladder U.S hastobedoneas soon as treatment
is initiated. IVP may or may not be done depending on
reliability and findings on U.S. Further evaluation with Mic
turating Cysto Ureterography (MCU) should be done after
therapy is completed in patients with suspected VUR. A
99Mc DMSAor DTPAscan may be required to consolidate
the findings and to detect the functioning renal tissue
when nephrectomy is considered.
In grade IV or V VUR surgery is indicated but it may be
delayed for months in infants and new born as reflux in them
is known to improve rapidly or even disappear.
The role or circumcision for prevention of UTI in neonates
is controversial. In the light of the epidemilogical observa
tions the American Academy of pediatric task force on
58
REFERENCES
1.
Ring E. Zobel G, UTI and malformation of Urinary tract in
Arch Dis Child 1988;63:818-820.
infancy.
2.
Duncan E Govan. David L Lark: Urinary tract infection in neonatesand
infants. Urologic surgery in neonates and young infants. Lowell R King. W.B.
Saunders Philadelphia 1989.
3.
Ian Winber: UTI in infants and children chapter 16 Campbells Urology
5th Edition 1986;738.
4.
G.D. Abbot UTI in children. Indian J Paediatrics 1986;53:81-86.
5.
Mark W. Burns, Jane L. Burns, John N. Kriegar: Paediatrics Urinary
tract infection diagnosis, classification arid significance. Paediatricclin North
Am 1987,34 1111
6.
Roleston GL, Shannor FT, Utley WLF : Relationship of infantile
vesicouretirc reflux to renal damage. Br med J 1970; 1:460
7.
Rolleston GL, Mating TMJ, Hudson CJ, Intrarenal reflux and thescarred
kidney. Arch Dis Chill 1974,49.531
8.
Secretory IgA in recurrent UTI in childhood. Editorial Lancet
1988;2(8608):433-434.
9.
Govan DE, Friedland GW, Fair WR et al: Management of children with
urinary tract infections. The Standford Experience
10. The natural history of recurrent bacteriuria in school girls N Engl J Med
1970;282:1443.
11. Fair WR, Goven DC: Influence of vesicouretral reflux on response to
treatment of urinary tract infections in female children. Br. J. Urol 1976:48:111
12. Wettergren B, Hellstrom M, Stokland E and Jodal M : six year follow up
of infants with bacteriuria on screening. Br. Med J 1990;30:845-848.
13. Williams DI, Johnson JH,: Paediatric Urology edition 2 butterworths
& Co London 1982;89-111.
14. Personal communication with Prof. T.P. Joseph. Department of Paedia
tric Urology, Calicut Medical College, Calicut.
15, Winberg J, Anderson HJ, Bergstrom T. et al: Epidemiology of sympto
matic urinary infection in childhood. Acta Pediatr Scand (suppl).
16. Joseph VJ, Chandrashekhara MK c'rcumcision. Does it prevent UTI?
Indian J Paediatr 1990;57:808-809.
VOL IV No. 3 & 4-----
ORIGINAL ARTICLE
St. John’s Medical College Journal of Medicine
ATTENUATION OF THE HAEMODYNAMIC RESPONSE TO
LARYNGOSCOPY AND TRACHEAL INTUBATION
IRIS RAJIVA, MARYOLLAPALLY
INTRODUCTION
Laryngoscopy and tracheal intubation, during light general
anaesthesia are frequently associated with hypertension
and tachycardia. This post intubation hypertensive res
ponse is particularly severe in the hypertensive. In these
patients there is an exaggerated response to many forms
of stress, in the conscious as well as in the anaesthetised
state.
Pharmacological attempts to attenuate the response have
included topical anaesthesia of the oropharynx, intravenous
lidocaine, adrenergic blocking drugs, vasodilating drugs,
calcium channel-blockers etc.
AIM
To compare the efficacy of sublingual nifedipine and topical
nitroglycerin in attenuating the haemodynamic response.
MATERIALS AND METHODS
On arrival at the operation theatre the pulse rate and systolic
pressure were recorded for all patients. A twelve lead ECG
system was also used and chest lead V5 was used for
recording ECG during the study period.
Ten patients received nifedipine 10 mg sublingually approxi
mately 10 minutes before the time of induction. These ten
patients constituted group I in our study. Group II patients
received nitroglycerin ointment topically. 2 inches spread
well and rubbed into the skin over an area of 6 inches to the
right of the sternum, covered with wax paper.
Anaesthesia was induced with thiopentone -5 mg Kg-1 in
order toobtund the eye lash reflex, followed by 66% nitrous
oxide and 33% oxygen. Pancuronium bromide 0.1 mgm/kg
was used to facilitate intubation. Laryngoscopy and
intubation were performed after onset of apnoea with a
Macintosh laryngoscope and took not more than 15-30
seconds. Following insertion of an appropriate sized en
dotracheal tube and inflation of cuff, anaesthesia was
maintained with a mixture of 33% oxygen and 66% nitrous
oxide till the study period was over.
This study was conducted on 20 hypertensive patients
undergoing elective surgery. All the patients had established
hypertension which had been adequately controlled preoperatively by drug therapy (diastolic pressure 100 mg Hg or
less). All patients belonged to ASA classification II.
The surgery was started only on completion of the study,
after which anaesthesia was conducted as per the surgical
requirements and patient requirements. The relevant data
was recorded in a specific Proforma made for this purpose.
The following parameters were recorded preoperatively :
1. Age (years) 2. Weight (Kilograms) 3. Systolic and diastolic
blood pressures (mm Hg) 4. Pulse rate (beats min-1
5. Electrocardiographic findings.
The following five parameters were computed at the
following instances for both the groups. 1. Pre-induction
value 2. During laryngoscopy (zero) 3. 1 minute after
laryngoscopy 4.3 minutes after laryngoscopy 5. 5 minutes
after laryngoscopy
Antihypertensive therapy was continued up to the day of
surgery. All patients were sedated with tablets diazepam
0.2 mg/kg body weight on the night before surgery. On the
morning of the surgery all patients received their anti
hypertensive medication (except diuretics) at 6 a.m. Pre
medication consisted of tablet Buprenorphine 0.4 mgm
sublingually, and tablet Phenergan 25 mgm orally -1 hour
before the expected time of induction.
All the parameters for each patient at each instant were
compared with their respective pre-operative values, which
was used as control value.
Observations and Results
Comparison of pre operative values with pre induction values.
Parameters
DR. IRIS RAJIVA
DR. MARY OLLAPALLY
DEPARTMENT OF ANAESTHESIOLOGY
ST JOHNS MEDICAL COLLEGE & HOSPITAL
BANGALORE-34
Oct - Dec 1991
Group I
Group II
+5.1 (21.94)
Pulse rate (beats min1)
+7.6(14.29)
Systolic pressure (mm Hg) +3.0(19.15)
-6 (11.55)
Diastolic pressure (mm Hg) -2.0 (8.16)
0 (12.15)
11.9 (38.21)
+2.67(11.22)
Mean arterial pressure
(mm Hg)
Rate pressure product
+1312(2923.6) +152(6192.56)
(beats mm Hg min1)
59 —
St. John’s Medical College Journal of Medicine
Comparison of pre operative values with values obtained during laryngoscopy
Group I
Parameters
Pulse rate (beats min1)
Systolic pressure (mm Hg)
Diastolic pressure (mm Hg)
Mean arterial pressure (mm Hg)
Rate pressure product
(beats mm Hg min1)
+ 28.4 (36.37)**
+ 8 (25.39)
+ 13.6 (20.37)*
+ 24.33 (49.29)
+ 5439.8 (7664.9)
Group II
+ 16.1 (24.36)#
-(16.33)
+ 11.0(16.67)*
+ 6.00(12.76)
+ 1755.0 (4379.49)
**P = <0.01 ; * P = < 0.05; # P = < 0.02
Comparison of pre operative values with values obtained one minute after laryngoscopy
Parameters
Group I
Group II
Pulse rate (beats min'1)
Systolic pressure (mm Hg)
Diastolic pressure (mm Hg)
Mean arterial pressure (mm Hg)
Rate pressure product
(beats mm Hg min'1)
+30.4 (41.09)**
+16(23.57)*
+12.4(15.69)*
26.93 (50.14)
+6662.0 (8614.29)**
+18.8 (30.59)#
1.0(10)
10(16.33)*
7.0(12.62)
3519.0 (6065.34)
**P <0.01 ;*P <0.05;#P <0.02
Comparison of Pre operative values with values obtained three minutes after laryngoscopy
Parameters
Group I
Group II
Pulse rate (beats min1)
Systolic pressure (mm Hg)
Diastolic pressure (mm Hg)
Mean arterial pressure (mm Hg)
Rate pressure product
(beats mm Hg min1)
+24 (32.42)**
+9 (22.85)
+7.2(16.87)
+15.801(42.88)
+4606.0 (6647.08)#
+18.8 (30.89)*
-16(25.39)*
-1.0 (8.82)*
-7.33 (12.67)**
+2359.0 (4417.02)
**P = <0.01 ; * P = < 0.05; # P = < 0.02
Comparison of pre operative values with values obtained five minutes after laryngoscopy
Parameters
Group I
Group II
Pulse rate (beats min1)
Systolic pressure (mm Hg)
Diastolic pressure (mm Hg)
Mean arterial pressure (mm Hg)
Rate pressure product
(beats mm Hg min'1)
+34.1 (44.13)**
-5.0 (22.36)
+1.4 (12.09)
+9.321 (34.9)
+3971.0 (33751.9)**
19.8 (28.04)#
-29.0 (34.48)*
-3.0 (8.82)
-9.99(12.86)**
-305.0 (3812.47)*
**P = <0.01 ; * P = < 0.05; # P = < 0.02
Conclusion
Nifedipine, a calcium channel blocker produces its action
of lowering blood pressure primarily by arterial vasodila
tion. Nitroglycerin on the other hand produces a fall in blood
press.ure by preferentially dilating the venous capacitance
vessels.
60
In conclusion wecan state that nitroglycerin ointment applied
topically (2 inches) 30 minutes before induction, offers an
advantage over sublingual nifedipine in attenuating the
pressor response to laryngoscopy and intubation in hyper
tensives.
VOL IV No.3 & 4-----
HEART RATE IN BEATS PER MINUTE
St. John's Medical College Journal of Medicine
DIASTOLIC PRESSURE IN mm Hg
SYSTOLIC PRESSURE IN mm Hg
TIME IN MINUTES
200
180
160
140
120
100
80
60
40
20
0
TIME IN MINUTES
Oct • Dec 1991
61 —
SELECTED SUMMARIES
St. John’s Medical College Journal of Medicine
SLEEP APNEA SYNDROME
K.M. NALINESHA
Sleep apnea is the cessation of air flow secondary either to
an obstruction of the upper air way or to a cessation of respi
ratory effort. By convention, air flow must stop for atleast 10
seconds to be considered an apneic event in adult.
Obstructive sleep apnea (OSA) was well described in the
classic Pick wickian syndrome (obesity, hypersomnolence)
in Charles Dicken’s classic work. The "Pickwick papers". In
1889, William Hill also recognised this syndrome with an
illustrative statement. "The stupid looking lazy kid who
frequently suffers from headaches at school, breathes
through his mouth instead of his nose, snores and is restless
at night, and wakes up with a dry mouth in the morning, is
well worthy of solicitous attention of school medical officer."
more common in REM sleep) (ENG) brain wave (electroen
cephalogram (EEG), Electrocardiogram (ECG), chest/abdominal respiratory movements, nasal or ora! airflow,
oxygen saturation (using ear lobe or finger oximetry) and
often a chin electromyogram (EMG). The study is ideally
performed overnight in a sleep laboratory.
INVESTIGATIONS
1.
Fiberoptic nasoendoscopy done at night provide
valuable information as to the site of obstruction in OSA.
2.
Imaging - lateral cephalometric x-ray of head and neck
gives information about site of obstruction.
A lateral high kilo voltage neck radiograph, taken in
phonation, is also useful is demonstrating velo pharyn
geal sphincter action and the relevant dimension of this
important region.
Sleep apnea syndromes are a common cause of excessive
day time sleepness and may lead to pulmonary
hypertension, systemic hypertension, cardiac arrythmias,
mental dysfunction, heart failure and sudden death.
The hypothesis for these changes was that the persistent
hypercarbia secondary to an inadequate respiratory effort
produced a type of carbon-dioxide narcosis, which
depressed the respiratory centre, resulting in extreme
sleepiness.
Etiologic aspects of OSA initially were thought to relate to
obesity and enlarged tonsils and adenoids. However cineradiographic studies and fibreoptic endoscopy of breathing
during sleep have shown that during respiration, the pharyn
geal wall collapses when obstructive sleep apnea occurs.
The electromyographic studies demonstrated clearly that
the obstruction is due to generalised relaxation of
pharyngeal musculature in the sleep apneic patient.
Drugs which may contribute to or cause sleep apnoea
syndrome include alcohol, sleeping pills, tranquillisers,
antiepileptic drugs and antihistamines. Withdrawl of these
drugs should be effected when evaluating the patient.
The diagnosis of sleep apnea is confirmed by a nocturnal
polysomnogram. This study consists of simultaneous
measurement during sleep of eye movement (electroocculogram) or electronystagmogram, (Sleep apnea is
DR. K. M. NALINESHA
ASST PROFESSOR
DEPARTMENT OF ENT
ST.JOHN'S MEDICAL COLLEGE HOSPITAL
BANGALORE - 560 034
CT Scan at the level of oro and hypopharynx can be
useful.
3.
Pulmonary function tests : Hypoventilation may be fully
evaluated when assessing OSA. The tests can be
positive for upper respiratory airway obstruction. Blood
gas analysis done along with the pulmonary function
study during sleep is of significance. (Usually normal in
the wakeful state.)
4.
Sleep latency tests - time taken by a subject to fall asleep
and monitored by an EEG, gives information on the
degree of excessive day time somnolence experienced
by the subject.
Sleep apnoea patients have a short sleep latency time,
usually less than 4 minutes. Normal value fall in the 615 minutes range.
TREATMENT: Medical
1.
Weight loss for the obese is of greater importance.
2.
Tricyclic antidepressant - protriptyline hag also pro
duced some improvements. (20 mg at night increased to
30 mg.)
3.
Tryptophan has been used in mild central sleep apnea
syndrome. (3 gm and 5 gm taken orally 30 minutes before
bed time.)
4.
Patients with hypoventilation and decreased ventilatory
drive may benefit from medroxy progesterone acetate,
VOL IV No.3 & 4 —
St. John’s Medical College Journal of Medicine
a respiratory stimulant. Average daily dose 60 mg 120 mg.
5.
Other drugs include acetazolamide, Nalosone without
conclusive results.
6.
High attitudes can exacelbrate the condition of OSA.
7.
Continuous positive airway pressure (PAP) has proved
most effective in the management of OSA. Obese indi
viduals, with a mixed apneic picture, often- benefit from
the therapy. Surgery is more risky since they are not
entirely obstructive. The equipment for nocturnal use
is now commercially available (in the West). It provides
a tight fitting nasal mask connected by a tubing to a quiet
pump. The mask is worn during sleep and the patient
quickly comes to relie on improved quality of sleep
achieved.
Oct • Dec 1991
SURGERY
1. Nasal surgery - correction of deviated nasal septum.
2. Uvulo-paluto pharyngoplasty - it involves resection of
1.5 cm of free posterior border of soft palate and
includes uvula posterior tonsilar pillars and part of
posterior pharyngeal wall medial to pillars, each side.
Tonsillectomy is also done if tonsils are present. This
help in 50% success in OSA and 95% in snoring.
3. Tracheostomy
4. Mandibular advancement
5. Genial tubercle advancement
6. Hyoid expansion
7. Hyoid suspension
8. Base of tongue resection
REFERENCE
OCNA - Ian S.Mackay, T.R.Bull, Rhinology - Scon Brown Otolaryngology,
5th edition August 1990.
63 —
REVIEW
St. John’s Medical College Journal of Medicine
HISTORY OF SURGERY - A BRIEF REVIEW
S.N. KOTHARE
ABSTRACT
of stone; by 1600 B.C. it was made of bronze and iron.'
This is a brief historical review of Surgery in Ancient Egyptian,
Indian, Chinese and Greek medicine, the Medieval, the
Renaissance and Post-Renaissance period and the Seven
teenth, Eighteenth and Nineteenth Century.
The Ebers papyrus of Egyptian medicine dates back to
1500 B.C. Its surgical section dealt with treatment of
carbuncles, cutaneous tumours, hernia, hydrocoele, etc.
Cautery was also used for checking excessive bleeding
during operations.2
HISTORY OF SURGERY
“Surgery is the first and the highest division of the
healing art, pure in itself, perpetual in its applicability, a
working product of heaven and sure of fame on
earth” - Sushruta (600 B.C.)
INTRODUCTION
Through the study of palaeopathology and recovery of
bones of prehistoric man, it is evident that diseases similar to
those of the present time, were also prevalent. There is
ample proof from recovered skulls that different methods
were employed in trephining as treatment for headaches,
epilepsy, etc. The purpose was to permit the “devil” causing
the disease to escape.1 Surgical instruments were made
of sharpened stones and flint. Further knowledge on the
subject of Surgery is derived from scripts written in
respective periods. Surgery, however, was practised in a
very limited manner. During the Roman period, frequent wars
gave an impetus to War Surgery, particularly traumatic
surgery.
ANCIENT TIME
The Egyptian practice of embalming the body contributed, to
a certain extent, to the knowledge of Anatomy, Surgery
and Bandaging. Among the ancient Egyptians circumcision of
males was practised as early as 5000 B.C. This was the
archaeological finding of Eliot Smith, in excavations of the
prehistorical cemetery of Naga-adder. Circumcision of the
prepuce of the clitoris in females was also practised. The
Edwin Smith papyrus is a surgical treatise probably written
some time between 3000-2500 B.C. It is, surprisingly, the
most important and complete treatise on Surgery of ancient
Egypt. It dealt essentially with traumatic surgery. The most
important surgical instrument of that time was the knife made
DR. S.N. KOTHARE, M.D. (BOM.)
D.T. M. & H.(LOND), F.A.C.T.M. (USA)
FORMERLY CONSULTANT-IN-CHARGE
HISTORY OF MEDICINE
ST. JOHN'S MEDICAL COLLEGE
BANGALORE 560 034
—
64
In ancient India advancement of surgery took place through
wars and battle wounds. Aryans used their knowledge of
herbal, mineral and other drugs effectively besides their
surgical skill. It is believed that Visapala, a woman related
to Raja Khela, accompanied him in the battle and lost a leg.
The Vedic surgeons Aswinis fitted her with an artificial leg.
Also described in Rigveda. the legend has it that Raja Bhoj’s
(980 AD) skull was trephined to relieve him of his severe
headache and to remove the malignant portion of the brain.
After the surgical procedure, the Raja was cured of the pain.2
Sushruta the greatest surgeon of ancient India had an
adequate knowledge of Surgery and also other branches of
medicine. Many surgical procedures were carried out,
including those on the abdomen; Skin grafting was also
carried out since Sushruta’s time. Vesical calculi, even
those days, were common and hence the operation for the
removal of vesical calculi was well described in Sushruta
Samhita. Surgical procedures for anal fistula, extraction of
foetus for abnormal presentations, amputations, excision of
tumours, repair of hernia and couching of cataract were
also known. Rhinoplasty was commonly performed for
restoration of severed or cut noses as punishment for
certain offences. Dr. Hirschberg of Berlin pays his tribute to
ancient Indian Surgery thus : “The whole plastic surgery in
Europe took a new flight when these punning devices of
Indian workmen became known to us.” The surgical
instruments were then made of iron. Several types of knives
and needles have been described depending upon their use
and tissues concerned.1
Sushruta the well-known surgeon of ancient i ridian medicine
is believed to have performed various operations mentioned
earlier. He taught his pupils how to make incisions on the
abdomen by using pumpkin for demonstration purposes. He
recommended the use of sharp surgical instruments made
of iron.1 It is recorded that the following indigenous method
for suturing fee severed ends of intestine was employed.
The cut ends of fee intestine were apposed to each other
arid big black ants (collected specifically for this purpose)
were made to bite fee apposed ends and their heads
severed when their pincers had closed. Thus the pincers
remained ‘in situ’ due to rigor mortis retaining the cut ends of
fee intestine in apposition for some time. The heads and the
pincers bl the ants being organic matter got digested in due
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St. John's Medical College Journal of Medicine
course of time, not unlike the catgut of the present-day
surgery Referring to ancient Indian medicine Castiglioni
writes “........... we must admit that Indian medicine, and
especially its surgery, had a development in ancient times
that was most probably quite independent of Greek
medicine "•
surgeon "A good surgeon should be acquainted with liberal
studies, with medicine and above all with anatomy ; he should
be courteous, bold in security, cautious in time of danger,
circumspect in prognosis, pious and merciful, not greedy of
gain, but looking for his fee in moderation, according to the
extent of his services.’’3
In ancient China Surgery was practised in a very limited
manner. Hua T’O (190 AD) has been quoted in ancient
Chinese medical scripts as the leading surgeon. In order to
produce eunuchs for the Imperial court, castration with
amputation of the penis was performed prior to 1000 B.C.
Chinese surgery apparently made no progress after the
advent of the Tang dynasty (619-907 A.D) due to strong
prejudices.1
SURGERY OF THE RENAISANCE AND POSTRENAISANCE PERIOD
In ancient Greek medicine reference is made to surgeons in
one of the Homeric poems written some time 1000 B.C.
Therein, it is stated "One surgeon was worth an army of
men.” recognising the value of a surgeon during frequent
wars that raged those days. It is also believed that
Hippocrates found in surgery rational methods of treating
certain diseases.3
MEDIEVAL TIME
Albucasis, an Arab, was born in Spain in the 10th century.
In ancient Arabic medicine he has been hailed as an
outstanding physician and an able surgeon. With special
instruments devised by him, he removed polypsand tonsils;
he frequently used branding iron and cautery in his surgical
practice. He also described obstetric instruments.3
Roger Frugardi of Salerno wrote the first western book on
Surgery in the year 1170; later it was reedited by his student
Ronald of Parma. Roger recommeded oral administration of
seaweed ashes for goitre, not unlike the present day iodine
therapy. His surgical skill is exhibited in his technique in
suturing severed intestines together over an elderwood tube
or an animal trachea.3
Theodoric de Lucea (1205-1248) postulated scrupulous
Cleanliness in surgical procedures as the basis of success.
Lanfrane, an Italian by birth, was educated in Milan; he
subsequently moved to Paris and settled down in practice as
a surgeon. He spread the Italian gospel of "healing wounds
by first intention" some time in 12953.
With the discovery of the gun powder in the 15th century and
the use of explosives in war weapons, extensive soft tissue
injuries and fractures of bones became quite common. The
nature and severity of wounds called for dexterity on the part
of the medical personnel and ingenuity for improvisation. In
fact war-time became a boom-time for surgeons with skill
and brains. Amongst these surgeons Ambroise Pare' (15101590) a voluntary field surgeon became an outstanding
surgeon of the 16th century. He wrote extensively on gun shot
wounds which was published as a treatise in 1545. He
advocated the use of ligatures to control bleeding and a
limited use of cautery in amputation, particularly in gun
powder wounds, with boiling oil. It is said that on the battle
field Pare' was considered equivalent to 10,000 troops
because soldiers believed that with Pare' around their chance
of survival was the greatest. He was a‘Barber Surgeon’ but
his skill and achievements were better than the so called
surgeons of those days. He was grudgingly admitted to the
‘College de St.Come’ despite the fact that he did not know
Latin3.
SURGERY DURING THE 17TH, 18TH AND 19TH
CENTURY/*5
In the 17th century, in England, Surgery was in the hands
of Barber Surgeons. They carried out simple procedures like
pulling out a painful tooth or even a complicated operation
such as amputation of the leg. For anaesthesia, they made
the patient unconscious by giving a knock on the head with
a wooden hammer.
During the eighteenth century several British men of
medicine contributed to the advancement of Surgery. Only a
few of these are mentioned here due to limitation of space.
Percival Pott (1713-1768) was famous for his treatise on
wounds, fractures and dislocations and less known for his
work on Hydrocele and Cafaract. One of the fractures is
known after him. As fate would have it, he sustained the same
fracture due to a fall from a horse-back4.
In England John Arderne (1307) established himself as a
reputed surgeon and later by 1376 became the pioneer
proctologist . He wrote a treatise on “Fistula-in-Ano and The
Use of Rectal Injections'’. He described his famous operation
for hemorrhoids,- excision of the thrombosed vein. He also
advised rectal examination to differentiate between fistulain-ano and anal cancer; the latter having a stony hard feel
to the examining finger.3
John Hunter (1728-93) was a great surgeon and an experi
mentalist. The production of "Hunterian Chancre”, experi
mentally on his forearm conclusively proved the etiology
and the contagious nature of Syphilis. Consequently he
developed Cerebral Syphilis as a late complication.4
Guy de Chauliac (1363) a renowned French surgeon in his
book "Great Surgery", .stipulated the qualities of a good
Astley Paston Cooper (1768-1841) was a student of John
Hunter. He had a passion for anatomy which brought him
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St. John’s Medical College Journal of Medicine
very near to body snatchers through whom he obtained
bodies for dissections. He made London as the surgical
centre of the world in the early 19th century. He was the
first to ligate the abdominal aorta. He successfully excised
a tumour from the head of king George IV for which he was
awarded baronetcy.4
More or less at this point of time the use of ether and
chloroform as anaesthetics turned out to be a milestone in
the development of complicated surgery. With the improve
ment of the technique of prolonged anaesthesia, surgeons
resorted to more complicated techniques as the duration of
the surgical operation was not any more an important factor.
However, deaths due to post-operative infection continued
to be a major obstacle.
James S.Syme (1799-1870) was born in Edinburgh. He
made several contributions to surgical literature. In 1823, in
Great Britain, he was the first to do drip exarticulation.4
Joseph Lister was his house surgeon in 1854, who derived
a lot of inspiration from his illustrious teacher.
The name of James Paget (1814-1899) is associated with
two conditions, Pagets disease of the nipple and Pagets
disease of bones4.
Joseph Lister (1827-1912) was a multifaceted individual. In
the early part of his career he described two distinct muscles
in the Iris, the dilator and the sphincter, and muscles in
the attached to hair follicles; contraction of these elevated
the hair resulting in goose skin appearance. In Glasgow his
attention was once again drawn to his previous observation
of frequent suppuration of wounds and gangrene. At this time
Louis Pasteur, in Paris, announced his discovery of the role
of germs in fermentation and putrefaction. On hearing of
this Lister also thought of the possibility of the presnce of
germs in wounds resulted in supparation and gaugrene. This
led him to search for a suitable antiseptic and he tried carbolic
acid for this purpose and succeeded in bringing down the
incidence of wound infection. His reputation as a great
surgeon spread all over Britain and also in Europe. In 1897
he was elevated to the peerage as Lord Lister for his surgical
achievements4.
Robert Liston in 1846, created a world record by performing
amputation of the leg in 33 seconds.5
In Germany, Christian Albert Theodor Billroth (1829-1894)
was making a name for himself through his surgical skill,
particularly of the gastro-intestinal tract. He in 1872, for the
first time resected the oesophagus; and in 1881, the first
resection of the pylorus for cancer. His name is associated
with several
operative
procedures.
Besides
his
professional achievements he was also an excellent pianist
and a great friend and admirer of Johannes Brahms4.
During this period, across the Atlantic Ocean, the American
medical faculty was also contributing to the advancement
surgery. James Marion Sims (1813-1883), an American by
birth, was a gynaecologist of repute. He described a surgical
66
procedure for repair of the Vesico-Vaginal fistula. The duck
bill vaginal speculum was also his creation.4
At this time in America Harvey Cushing (1869-1939) was
hitting the headlines as a Neurosurgeon. He published his
observations on the role of Pituitary tumours and sexual
infantilism which was further supported by experimental
work. His classical publication on ‘The Pitutary Body and
Its Disorders’ is a masterpiece of meticulous observations
and their correlations. He was a prolific writer. He published
interesting papers on medical history including a biography
entitled “The life of Sir. William Osler.4
Subsequently, Surgery made rapid strides in the latter half
of the 19th century and the early part of the 20th century,
consistent with rapid advances in basic sciences. Asa result,
specialization in surgery was envisaged and introduced to
improve the quality in surgical practice. Due to constraint of
printing space adequate coverage of several eminent
surgeons of this period is not possible
The most outstanding surgical achievement in the latter half
of the twentieth century is 'Transplant Surgery’.
Attempts at transplant of the skin were made by Sushruta. In
303 AD the twin brothers, Cosmos and Damian, physicians
of Arab origin, amputated the leg of a Caucasian and
attempted to graft in its place the leg of a recently deceased
Moor. John Hunter successfully transplanted the spur on the
cock’s comb. With this was reborn the concept of transplants
of tissues and organs. In the year 1905, organ transplant was
attempted by Alexis Carrel, a French surgeon, - an autotrans
plant of a dog kidney. Although the attempt was unsuccessful,
in 1912, he was awarded the Nobel prize in medicine for this
experiment. The first heart transplant was performed by
Dr. Christian Brnard of South Africa in the Groot Shuar
Hospital. Capetown, on the 3rd Dec. 1967. In India the first
heart transplant was performed at the King Edward VII
Memorial Hospital, Bombay on the 16th Feb. 1968 by the late
Dr. Prafulla Kumar Sen, who was then the Professor and
Head of the department of Cardiothoracic surgery.6 Similar
other organ transplants are being undertaken such as that of
kidney, lung, bone marrow, etc. The first kidney transplant at
K.E.M. Hospital, Bombay was performed in the year 1960.
The first successful Renal Transplant was performed at
Christian Medical College, Vellore in the year 1971.
REFERENCES
1.
2.
3.
4.
5.
6.
Castiglioni, A.: A History of Medicine, published by Alfred A Knopf Inc.
First American Edition, 1941 pp.13, 17,50,54.90,92,104.
Bhatia, Maj. Gen. S.L : A History of Medicine with special reference to
the Orient, published by Medical Council of India 1977, pp. 50,84,85
Bettmann, OL : A Pictorial History of Medicine. Charles C, Thomas,
Publisher, Springfield, Illinois, pp. 14.15,23.60,61,68,69,78,79,81,84.
Major, Ralph H : A History of Medicine Charles C. Thomas Publishers.
Springfield, Illinois U.S A.Vol2pp635.659.692.761,816,821,879.894,895.
The Golden Age of Surgery : The Surgical Clin, of N Amer. Vol 58/No 5
Oct, 1978. p. 931-32.
Personal Communication Dr. Kinare. S.G. Professor of Pathology
(Retd.) SEth G.S. Medical College and K.E.M Hospital Parel, Bombay
4000 012.
VOL IV No.3 & 4-----
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