Diabetes mellitus -Clinical features and Management

Clinical features:
Type1 DM Symptoms: General age of presentation is less than 20 yrs. Osmotic symptoms like polyuria, polydyspsia, polyphagia are the presenting features. Weight loss is very common. May present with features of D !. "amily history of DM may or may not #e present. Signs: $ow %M& is very characteristic. 'vidence of infection in the form of furuncles, respiratory infections may #e present. 'vidence of other autoimmune disorders like graves, addison(s, vitiligo may #e present. Type 2DM Symptoms: )lassical age of presentation is a#ove *0yrs. May #e detected on routine e+amination. ,resenting symptoms may #e infections like vulvovaginitis, #alanitis, and pneumonia. D ! as presenting feature is very rare unlike type- DM. .ype2DM unlike type- may present with chronic complications of dia#etes. 1) ,rogressive loss of vision, sudden loss of vision, fre/uent change of glasses000 diabetic retinopathy. 2) ,edal edema, facial puffiness, and hypertension0000 diabetic nephropathy. ) %urning sensation in the feet and hands isolated cranial nerve palsy, pro+imal muscle weakness 000 diabetic neuropathy. !) 'rectile dysfunction, urinary incontinence, nocturnal diarrhoea, giddiness on standing 000autonomic neuropathy. ") 1istory of #$D and C%&. ') 1istory of claudication2peripheral vascular disease and foot ulcers 000 diabetic foot. "amily history is generally strongly positive. ,ersonal history 3 history of sedentary life, lack of e+ercise, smoking, and alcohol should also #e asked. &n all cases of dia#etes following /uestions should #e asked 1) When and how DM was diagnosed. 2) &s the patient following proper diet and e+ercise. ) what drugs were prescri#ed and any side effects4including insulin5 !) 1ow fre/uently sugars are #eing checked. Signs: (M# generally is more than 264obesity5. Waist hip ratio 7 0.8. 4normal women 90.: ; men 90.85

)allor2may #e feature of )<" due to dia#etic nephropathy. *ymphadenopathy000 may #e a feature of occult infection like tu#erculosis. )edal edema 000 possi#le causes are nephropathy, ))", drugs like amlodipine, pioglita=one. May give clue for cause of dia#etes like steroid induced )ushing(s syndrome etc. )ulse 3 resting tachycardia 4autonomic neuropathy5, a#sent peripheral pulses 4,>D5, carotid #ruie and thickened vessel wall 4atherosclerosis5. (lood pressure? standing and lying %, should #e taken in all dia#etic patients. Postural hypotention may #e a suggestive of autonomic neuropathy, side effect of drug like clonidine, !)' inhi#itors. usssmausal(s #reathing may #e seen in D !. Other general e+aminations features include? 1) +anthomas and +antholesma,s 4feature of hyperlipidemia5. 2) Oral candidiasis, thyroid swelling 4thyroiditis as in type -DM5. ) "acial puffiness 3 nephropathy, secondary causes like )ushings syndrome. !) &canthosis nigricans 3 velvety pigmentation commonly seen on #ack of the neck, a+illa and groin regions. ") 1ands 3 look for dupytren(s contracture, carpal tunnel syndrome, and prayer(s sign. ') $ipoatrophy and dystrophy at the insulin in@ection sites. -) Diabetic dermopathy 4hyperpigmented patches seen on shin5 necro#iosis lipoidica 4on shin5. .) "oot for ulcers on the pressure sites and fungal infections. /) )harcot @oints. (M# 0 2"1 2aist hip ratio 0 3./ and acanthosis nigricans are features of insulin resistance. C%S: 4eatures of #$D 5 hyperdynamicape+, AB, dyskinatic segment, and M< murmur. "eatures of 1.Csive heart disease 000 heaving ape+, loud !2, A*, 'AM in aortic area. &bdomen: 1epatomegaly2fatty liver, ))". !scitis 3 ))", nephropathy. '+ternal genitalia for infections <enal #ruie. 6espiratory system: #asal crepitations000))" and fluid over load states like nephropathy. Aigns of pulmonary .%. C7S: "undus for dia#etic retinopathy and hypertensive retinopathy. )ranial neuropathies esp. B,* D Motor system000 lower lim# pro+imal muscle weakness4amyotrophy5 Aings of sensory motor neuropathy 3 fine touch 4#y monofilament5, vi#ration 4-2:h= tuning fork5, @oint position sensation and rhom#erg(s sign, pain sensation #y needle.

refle+es esp. ankle and knee @oint. >i#ration sensation is the first sensation to #e lost in dia#etics. Aigns of stroke. One micro or macro vascular complication look for other micro or macro vascular complications. '.g nephropathy is very commonly associated with retinopathy. !therosclerosis at one site look for atherosclerosis at other sites.

4C)D 84ibrocalculous )ancreatic Diabetes) )ommon age of presentation is 200*0 yrs. Aymptoms and presentation is similar to type - DM #ut diarrhoea and pain a#domen may #e a predominant feature.
IDDM 1. 2. 3. Usual age at onset (years) Sex "re#alen$e 5-30 M:F = 1:1 Type 2 DM 35-65 FCPD 10-30 M>F 6!t0!n t0e tro%!$s 1ore !n $assa#agro4!ng areas 2ot esta,l!s0e 3ean( e1a$!ate Slo4( a, o1!nal $ol!$ !n 1any 2ot %rone :,sent 99

7. 5. 6. =. *. .. 10. 11. 12. 13.

8enet!$ 2utr!t!on (,u!l ) Usual onset >etos!s Islet $ell ant!,o !es Insul!n la$5 Insul!n res!stan$e Insul!n re?u!re1ent Sul%0onylurea )o11on $auses o& eat0

F>M In !a: M > F More !n %o%ulat!ons o& .0-.5+ o& all 'uro%ean or!g!n( !a,et!$s. )au$aso! s (5-*+ o& /!g0est !n "!1a all !a,et!$s). In !ans( 2aurans. 1+ !n In !a( -a%an 3o4 !n 's5!1oes( tr!,als /ere !ty 9 strong /3: /ere !ty 9 9 9 2o asso$!at!on /3: asso$!at!on 2on-o,ese ;&ten o,ese( 1ay ,e non-o,ese or lean( %art!$ularly In !ans <a%! Slo4( !ns! !ous "rone 2ot %rone

"resent 4!t0!n 1 year :,sent o& onset 9999 9(-)

<are( se$on ary 40en 9 9 9 %art!$ularly !n 9 9 %resent o,ese 3o4 to 1o erate 3o4( 1o erate to 0!g0Mo erate Unres%ons!#e <es%ons!#e <arely res%ons!#e 2e%0ro%at0y( )/@( )/@( ne%0ro%at0y( 3a$5 o& 5etoa$! os!s( stro5e( treat1ent gangrene 0y%ogly$ae1!a

*aboratory 4indings Criteria for diagnosis is already disused (ase line in9estigations to be done in a patient diagnosed as DM for the first time: 1) "%A,,,%A, Gly 1# 2) 1emoglo#in. ) Erea, creatinine, Ca, . !) Erine for microscopy and al#uminuria. ") "asting lipid profile. ') ')G. -) Other investigations if re/uired 000 )F< 4pulmonary .%5

)0peptide and insulin levels 4to differentiate type- and type2, increased in type 2 Eltrasound a#domen and +0ray a#domen2"),D.

:lycosylated $b: 1emoglo#in #ecomes glycated #y ketoamine reactions #etween glucose and the free amino groups on the and chains. .his glycated 1# portion can #e measured as 1# !- . .he ma@or form of 1#!- is hemoglo#in !-c 41#!-c5. Aince glycohemoglo#ins circulate within red #lood cells whose life span lasts up to -20 days, they generally reflect the state of glycemia over the preceding :3-2 weeks, there#y providing an improved method of assessing dia#etic control Ahould never #e used for diagnosis #ut is the #est investigation for follow up. &deal value of 1#!-c is less than GH. !n increase in -H of 1#!-c reflects increase in sugar app+. *0mgIdl. !ny condition that shortens erythrocyte survival or decreases mean erythrocyte age 4eg, recovery from acute #lood loss, hemolytic anemia5 will falsely lower 1#!-c Serum fructosamine Aerum fructosamine is formed #y nonen=ymatic glycosylation of serum proteins. Aerum fructosamine generally reflects the state of glycemic control for only the preceding -32 weeks Self-monitoring of blood glucose )apillary #lood glucose measurements performed #y patients themselves, as outpatients, are e+tremely useful. .here are several paper strip 4glucose o+idase, glucose dehydrogenase, or he+okinase5 methods for measuring glucose on capillary #lood samples. Continuous glucose monitoring systems )ontinuous glucose monitoring systems are currently availa#le for clinical use. &t involves inserting a su#cutaneous sensor that measures glucose concentrations in the interstitial fluid for G2 hours.

M&7&:;M;7T <4 DM .he goals of a successful dia#etes programme a5 O#tain faster symptomatic relief, #5 <educe if not to prevent the microangiopathic complications, c5 Minimise the risk factors associated with macrovascular disease, d5 !ctively involve the patient in dia#etic care through continual education and e5 !ttain and preserve an e+cellent /uality of life #y adopting a healthy life0style :oals of diabetes therapy #7D;+ 1#!-c ,reprandial plasma glucose ,eak postprandial plasma glucose 1yperlipidemia :<&* 9 G.0H 803-B0 mgId$ 9-:0 mgId$ $D$ 9 -00 mgId$ ,.G 9 -60 mgId $1D$ 7 *0 mgId$

.here are three modes of treatment of DM. 1) Diet and '+ercise. 2) Oral hypoglycemic agents 4O1!5 ) &nsulin .ype of therapy is #ased on circulating plasma insulin concentration. .herapy of dia#etes is for life long. &5 Diet !ttainment of optimal #ody weight results in marked diminution of hyperglycaemia and increase in target cell response to insulin. &deal #ody weight 4&%W in kg5 J 4height in cm 0 -005 + 0.8..he o#ese and the overweight must #e encouraged to lose weight "or o#ese patients weight loss of .6 g per week should #e aimed.

Calorie inta=e is based on acti9ity.

Aedentary work 0 20026 calsI g of &%W, Atrenuous work 0 B-0B6 calsI g of &%W. Distribution of nutrients in diet: )ar#ohydrates 0 D0 to D6H , ,roteins 0 -6 to 20H, "ats 0 -6 to 26H :lycaemic inde>?it is ratio of glucose level after taking a particular food to that of glucose of same /uantity. "oods of low glycaemic inde+ are preferred. "i#er rich diets 4cellulose, pectin of plants5 are advised as they reduce rapid swings of glucose levels. &ndian food is rich in fi#er. !ttention should #e paid for the type of fat taken #y the patient. !rtificial sweeteners 4saccharin and aspartamate5 are availa#le #ut costly alternative. "resh fruits can #e taken #ut not @uices.

 !void alcohol and smoking. <educe salt intake to less than Dgrms per day if patient has hypertension. ;>ercise: &t improves glycaemic control #y reducing insulin resistance, #ody weight and risk factors for )!D !ero#ic e+ercises like walking, swimming and cycling are #etter. %risk walking for -I2hrIday is sufficient. ,atients on insulin should have snacks #efore strenuous e+ercise.

Complications of diabetes mellitus

# &cute -. Meta#olic and Subacute 2. &nfections etoacidosis coma 1yperosmolar non0ketotic coma $actic acidosis 1ypoglycaemia %acterial, fungal? Akin, mucosa, soft tissues, urinary tract, lungs, #one

##. Chronic -. Macroangiopathy )oronary heart disease, cere#rovascular disorders, peripheral vascular disease 2. Microangiopathy <etinopathy, nephropathy, dermopathy, Ceuropathy *. Miscellaneous Dia#etic foot, cardiomyopathy, ocular complications other than retinopathy, erectile impotence.

ACUTE COMPLICATIONS OF DM !cute complications of DM include 1) Dia#etic ketoacidosis 4D !5 2) Con ketotic hyperosmolar coma 4C 1)5 ) 1ypoglycemia. !) $actic acidosis D#&(;T#C @;T<&C#D<S#S 8D@&) D ! is medical emergency and mortality is a#out 60-0 H. )ardinal features are 1) 1yperglycemia

2) 1yperketonemia ) Meta#olic ketoacidosis )athophysiology D ! results from relative or a#solute insulin deficiency com#ined with counter regulatory hormone e+cess 4glucagon, catecholamines, cortisol, and growth hormone5. .he decreased ratio of insulin to glucagon promotes gluconeogenesis, glycogenolysis, and ketone #ody formation in the liver, as well as increases in su#strate delivery from fat and muscle 4free fatty acids, amino acids5 to the liver. etosis results from a marked increase in free fatty acid release from adipocytes, with a resulting shift toward ketone #ody synthesis in the liver. etones produced are #eta hydro+y #utyric acid, acetone and acetoacetate.

Clinical featuresSymptoms CauseaIvomiting )hysical findings .achycardia

.hirstIpolyuria !#dominal pain Ahortness of #reath

Dehydration and hypotension .achypneaI ussmaul respirations !#dominal tenderness 4may resem#le
acute pancreatitis or surgical a#domen5 O#tundation

)oma

)recipitating e9ents &nade/uate insulin administration

&nfection 4pneumoniaIE.&IgastroenteritisIsepsis5 &nfarction 4cere#ral, coronary, mesenteric, peripheral5 Drugs 4cocaine5 ,regnancy

Differential diagnosis Aimple hyperglycemia 1yperglycemic hyperosmolar state Atarvation ketosis !lcoholic ketoacidosis *aboratory &bnormalities D ! is characteri=ed #y hyperglycemia, ketosis, and meta#olic acidosis 4increased anion gap5 Erine !cetoacetate is detected #y used ketosis detection reagent 4nitroprusside5 Aerum potassium at presentation may #e mildly elevated. 'levated #lood urea nitrogen 4%EC5 and serum creatinine levels reflect intravascular volume depletion $eukocytosis, hypertriglyceridemia, and 1yperamylasemia4salivary origin 5are commonly found as well.

Management of Diabetic @etoacidosis

)onfirm diagnosis 4K plasma glucose, positive serum ketones, meta#olic acidosis5. !dmit to hospitalL intensive0care setting may #e necessary for fre/uent monitoring or if p1 9 G.00 or unconscious. !ssess? Aerum electrolytes, !cid0#ase status, urine ketones, renal function a) 4luid replacement: 4luid 0 0.8H saline 4Ca)l5 i.v.

6ate 0 - liter over B0 minutes followed #y - liter over - hr, - liter over 2 hrs, - liter
over ne+t 20* hrs When #lood glucose 9 2G0 mgIdl Awitch to 6H de+trose, - litre :0hourly

.ypical re/uirement is D litres in first 2* hrs #ut avoid fluid overload in elderly
patients Au#se/uent fluid re/uirement should #e #ased on clinical response including urine output b) #nsulin 60 unit(s solu#le 4plain5 insulin in 60 ml 0.8H saline i.v. via infusion pump D unitsIhr initially followed #y B unitsIhr )heck #lood glucose hourly initially0if no reduction in first hour, rate of insulin infusion should #e increased

 !im for fall in #lood glucose of 660--0 mgIdl per hour

c) Serum potassium &f plasma potassium 9 B.6 mmolIl, give *0 mmol of )$ per - litre of fluid

&f plasma potassium is B.606.0 mmolIl, give 20 mmol of )$ per - litre of fluid &f plasma potassium is 7 6.0 mmolIl, give no added potassium
ADDITIONAL PROCEDURES IN THE MANAGEMENT OF DIABETIC KETOACIDOSIS )atheterisation if no urine passed after B hrs Casogastric tu#e to keep stomach empty in unconscious or semiconscious

patients, or if vomiting is protracted )entral venous line if cardiovascular system compromised, to allow fluid replacement to #e ad@usted accurately ,lasma e+pander if systolic %, is 9 80 mm1g or does not rise with i.v. saline !nti#iotic if infection demonstrated or suspected ')G monitoring in severe cases )ontinue a#ove until patient is sta#le, glucose goal is -603260 mgId$, and acidosis is resolved. &nsulin infusion may #e decreased to 0.0630.- unitsIkg per hour. !dminister intermediate or long0acting insulin as soon as patient is eating. !llow for overlap in insulin infusion and su#cutaneous insulin in@ection.
)ere,ral oe e1a- Areat 4!t0 1ann!tol( oxygen :$ute res%!ratory !stress syn ro1e A0ro1,oe1,ol!s1 @!sse1!nate !ntra#as$ular $oagulat!on (rare) :$ute $!r$ulatory &a!lure

Complications

7on =etotic $yperosmolar coma 87@$C) C 1) is characteri=ed #y severe hyperglycemia and with or without significant ketoacidosis. More common in elderly and mortality is a#out 600:0H. >arious differences #etween D ! and C 1) are given the #o+.
"las1a glu$ose (1gB l) "las1a 5etones DKA 350-*50 9999 (25-100 1gB l 5-20 11olBl) 3o4C 'le#ate ( nor1al( 1ay ,e lo4 E 10 > 12 E =.3 HONC *00-1600 9

Seru1 so !u1 "otass!u1 D!$ar,onate (1'?Bl) :n!on ga% (1'?Bl) Dloo %/

<a!se (>170 1'?B1) <a!se Bnor1al > 1* 10-12 2or1al

;s1olal!ty (1;s1Bl) <a!se ,loo urea n!trogen /ae1ato$r!t ( e0y rat!on)

E 330 9 999

370-350 99 9999

1) Serum osmolality 5 24Ca M 5 MureaI6.D MglucoseI-:.normal serum osmolality is 2:00 B00 mosmolsIkg 2) &nion gap 3 4Ca M 5 3 4)l M 1)OB5. Cormal anion gap is -00-2. !G is markedly increased in D ! #ut normal to high in C 1). Management: Management of C 1) is same as D ! with some differences 1) C 1) is very sensitive to insulin so half the dose of insulin is used. 2) Ahould use .*6H of Ca)l until serum osmolality is normal then normal 4.8H5 saline can #e used. N 1ypoglycemia is discussed in detail later. N $actic acidosis in dia#etic patients can #e caused due to infection or metformin.

C$6<7#C C<M)*#C&T#<7S <4 DM

)athogenesis "our theories have #een proposed to e+plain how hyperglycemia might lead to the
chronic complications of DM -5 "ormation of advanced glycosylation end products 4!G's5 via the nonen=ymatic glycosylaton of intra0 and e+tracellular proteins. 25 &ncrease glucose meta#olism via the sor#itol pathway B5 "ormation of diacylglycerol leading to activation of protein kinase ) 4, )5 *5 hyperglycemia increases the flu+ through the he+osamine pathway, which generates fructose0D0phosphate..his alters the function #y glycosylation of proteins. !ny of the a#ove one or more therioes lead to altered cell functions, renal and vascular connncetive tissue changes etc finally leading to vacular damage thus resulting in chronic complications of dia#etes.

.he Dia#etes )ontrol and )omplications .rial 4D)).5,

.he Enited ingdom ,rospective Dia#etes Atudy 4E ,DA5 and umamoto study prove the value of meta#olic control and emphasi=e the importance of 4-5 intensive glycemic control in all forms of DM, and 425 early diagnosis and strict #lood pressure control in type 2 DM.

Dia#etic nephropathy is the most important cause of 'A<D all over the disease. >arious stages of dia#etic nephropathy are 1) Atage of hyperfiltration 2) Atage of microal#uminuria 4B00B00micrograms of al#uminIday5 ) Atage of overt proteinuria. During this stage patient may have nephrotic range of proteinuria.

Diabetic nephropathy

!) 'nd stage renal disease4'A<D5 ,attern of progression of dia#etic nephropathy

,athological changes include thicking of glomelular #asement mem#rane and later nodular deposits with glumeruloscerosis 4 immelsteil0wilson lesion5. immelsteil0 wilson is very typical of dia#etic nephropathy. Clinical features )linical manifestation are representation of hypoal#uminemia ,edal edema, facial puffiness, pleural effusion, ascitis 'tc. #n9estigations 1) Erine for microal#uminuria 3 . Microal#uminuria is defined as B0 to B00 mgId in a 2*0h collection or B0 to B00 OgImg creatinine in a spot collection 2) Eltra sound a#domen to rule out o#structive uropathy and other causes of renal failure. ) <enal functions and electrolytes. !) &nvestigations to rule out other complications. Management: 1) !ggressive control of %,. .arget %, should #e #elow -20IG6. Drug of choice for dia#etic nephropathy with or with out hypertension are angiotensin0converting en=yme 4!)'5 inhi#itors e.g ramipril ,enalapril, angiotensin receptor #lockers 4!<%s5 '.g losartan,valsaltan etc. theses drugs are used if !)' inhi#itors have side effects and can also #e added to !)' inhi#itors is %, target is not reached. .hese drugs not only reduce the %, #ut also reduce the proteinuria. .hese drugs are contra indicated in presence of renal failure. 2) .ight control of sugars. !void using metformin if there is renal failure. &ncidence of renal failure, dose of insulin will come down markedly.

B5 Acreen for dia#etic retinopathy and other complications. *5 !void nephroto+ic drugs and treat E.&. ") <enal replacement therapy 4dialysis and renal transplantation5 is re/uired for patients with 'A<D.

Diabetic neuropathy
'ffects B0H of dia#etics. ,athogenesis includes a+onal degeneration and damage to vasa nervosum. Classification !5 Aomatic ,olyneuropathy a5 Aymmetrical, mainly sensory and distal #5 !symmetrical, mainly motor and pro+imal 4including amyotrophy5 Mononeuropathy 4including mononeuritis multiple+5 %5 >isceral 4autonomic5 )ardiovascular, Gastrointestinal, Genitourinary Clinical features 1) Aymmetrical sensory polyneuropathy? ,arathesia of feet and hands 4glove and stocking distri#ution5. Muscle wasting and weakness are late features. Aensory loss and loss of D.< are the main features. >i#ration sensation 4-2:1=5 is the first sensation to #e lost. May develop foot ulcers4dia#etic foot5 and charcot @oints5 2) !symmetrical dia#etic motor neuropathy? )alled as dia#etic amyotrophy. )auses progressive weakness and wasting of pro+imal muscles. Weakness is asymmetrical and painful. %ut prognosis is good. ) Mononeuropathy? Aingle peripheral nerve palsy. May mimic hensen(s disease. )ranial nerve palsies are also common esp. Brd and Dth nerves. .horacic nerves can also #e affected. )arpaltunnel syndrome can also #e feature of DM. !) !utonomic neuropathy? Cardio9ascular- ,ostural hypotension, <esting tachycardia Gastrointestinal 0 Dysphagia, Cocturnal diarrhoea or )onstipation :enitourinary 0 urinary incontinence, 'rectile dysfunction and retrograde e@aculation <thers 3 Audomotor, vasomotor Management of neuropathy Ata#ili=ation and optimi=ation of glycemic control !voidance of neuroto+ins 4alcohol, drugs5

Aupplementation with vitamins for possi#le deficiencies 4vitamin %-2 , vitamin %D , folate5 Treatment of painful neuropahty -. .ricyclic antidepressants0 !mitriptyline 4263-60 mg ,O at #edtime5 2. Aerotonin reuptake inhi#itor0Dulo+etine B. !nticonvulsants0 Ga#apentin 4B003D00 mg ,O tid5, )ar#ama=epine *. Opioid or opioid0like drugs0 .ramadol 4603200 mg ,O #id5 6. )apsaicin cream 40.0G6H5 0.opical analgesic applied to painful areas * times daily Treatment of <rthostatic hypotension -5 Oral "ludrocortisone 25 Con pharmacologic maneuvers may offer some #enefit. !de/uate salt intake !voidance of dehydration and diuretics $ower0e+tremity support hose Graded supervised e+ercise 'rectile dysfunction0 Aildenafil "oot care D#&(;T#C 4<<T ;tiology: .rauma 4trivial5 in presence of neuropathy and ,>D 000ulcer and infection. Ceuropathy or ischaemia or #oth can cause dia#etic foot. C*#7#C&* 4;&TA6;S <4 T$; D#&(;T#C 4<<T 7europathy #schaemia Symptoms Cone Cone ,araesthesiae )laudication ,ain <est pain Cum#ness Structural damage Elcer Elcer Aepsis Aepsis !#scess Gangrene Osteomyelitis Digital gangrene )harcot @oint M&7&:;M;7T <4 D#&(;T#C 4<<T A*C;6S <emove callus skin .reat infection !void weight0#earing 'nsure good glycaemic control

)ontrol oedema Endertake angiogram to assess feasi#ility of vascular reconstruction where indicated. )!D, ,>D and )>! are not disscused.

SA6:;6B &7D D#&(;T;S !ll patients undergoing surgery 000 cata#olic stress leading to cortisol and catecholamines and glucagon. .hese hormones increase glucose levels and increase insulin resistance and predispose the patient to D ! esp. if the sugars are uncontrolled #efore the surgery. &ncrease in glucose levels also delays the wound healing, so increase the post operation complications. Details of the management of the patient #efore and during the surgery are given the #o+.

&) () 1) 2) ) !)

)6;:7&7CB &7D D#&(;T;S )regnancy in a diabetic patient. Encontrolled sugars during pregnancy can cause fetal a#normalities and increase in the perinatal mortality rate. Management of the dia#etics during pregnancy is given the #o+. :estational diabetes Def? 1yperglycemia diagnosed first time in pregnancy. <isk factors age 726 %M& 726 ,ast history of gestational dia#etes. family history of DM !ll pregnant women who are at risk should #e screened. .esting for GDM should #e done #etween 2*02:weeks.

T2o step method 1) Step one: 60gms of oral glucose 4any time of the day5. .hen venous plasma sugars after one hour. Cormal 9-*0mgHL if the value is 7-*0mgH proceed to step two. 25 Step t2o: :hrs of fasting --- -00gms of glucose orally then draw plasma venous sample at 0,-,2,B hrs. 2 or more a#normal values 3 diagnostic of GDM 1) fasting 3 86 mgIdl 2) -hr 00 -:0 mgIdl ) 2hrs 000 -66mgIdl !) Bhrs 000 -*0mgIdl Management: ,lan early delivery 3 BD0B:weeks due to increased risk of &ED. !void O1! and control the sugars #y insulin. Maintain the sugars #elow -06mgIdl. On the day of delivery stop insulin and start glucose and insulin and infusion and monitor sugars 20B hrs. Maintain the sugars #etween 800--0 mgIdl. "ollow0up of the patients with GDM is very important, as they have increased risk of developing DM. C$;C@*#ST 4<6 4<**<C-A) <4 )&T#;7TS C#T$ D#&(;T;S M;**#TAS Arinalysis 0 al#umin 4#oth macro0 and microal#uminuria5, ketones :lycaemic control 0Glycated haemoglo#in 41#!-c5 ,"%A, ,,%Aand inspection of home #lood glucose monitoring record

 $ypoglycaemic episodes Cum#er of episodes and fre/uency .ime of day when PhyposP e+perienced (lood pressure 3 fre/uent monitoring of %, esp in patient with nephropahty ;ye e>amination *o2er limbs ,eripheral pulses ,.endon refle+es ,erception of vi#ration sensation, light touch and proprioception 4eet )allus skin indicating pressure areas ,Elceration #n9estigation for #$D ')G and stress testing and echocardiogram 4asting lipid profile "$, should #e done once in B0D months #n9estigate for contrainfications for drugs e.g 3 $". for gita=ones