Diabetic Complications and Emergencies

8/7/2019 Diabetic Complications and Emergencies

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DIABETICDIABETICCOMPLICATIONS ANDCOMPLICATIONS AND

EMERGENCIESEMERGENCIES


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Pathophysiology of DiabeticPathophysiology of DiabeticComplicationsComplications

Pathophysiology of micro and macro vascular complications is ill defined. Follwing consequences of Pathophysiology of micro and macro vascular complications is ill defined. Follwing consequences of hyperglycemia may play a role.hyperglycemia may play a role.

Non enzymatic glycosylation of a wide variety of proteins lead to accumulation of Non enzymatic glycosylation of a wide variety of proteins lead to accumulation of AGE AGE ( Advanced Glycosylated End products) causing injury via stimulation of pro inflammatory( Advanced Glycosylated End products) causing injury via stimulation of pro inflammatoryfactors e.g complement, cytokines.factors e.g complement, cytokines.

Polyol pathwayPolyol pathway : Metabolism of glucose by increase aldose reductase lead to accumulation: Metabolism of glucose by increase aldose reductase lead to accumulationof sorbitol and fructose that causes changes in vascular permeability , cell proliferation andof sorbitol and fructose that causes changes in vascular permeability , cell proliferation andcapillary structure.capillary structure.

Micro vascular occlusion due to vaso constrictors (endothelins) lead to impaired supply of Micro vascular occlusion due to vaso constrictors (endothelins) lead to impaired supply of nutrints and oxygen.nutrints and oxygen.

Other factors like reactive oxygen species , VEGF and TGFOther factors like reactive oxygen species , VEGF and TGF beta released by ischemic tissuesbeta released by ischemic tissuescause endothelial cell proliferation.cause endothelial cell proliferation.

Hem odyna mic chang es in k idn e ysHem odyna mic chang es in k idn e ys : includes raised glomerular filtration rate , increased: includes raised glomerular filtration rate , increasedintra glomerular pressure , mesangial cell hypertrophy and increased secretion of extraintra glomerular pressure , mesangial cell hypertrophy and increased secretion of extracellular mesangial matrix leading to glomerular sclerosis and thickening of basement cellular mesangial matrix leading to glomerular sclerosis and thickening of basement membrane that leads to disruption of protein linkages and leak of large molecules (especiallymembrane that leads to disruption of protein linkages and leak of large molecules (especiallyproteins into the urine).proteins into the urine).


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COMPLICATIONSCOMPLICATIONS

MICROVASCULARMICROVASCULAR

1.1.RetinopathyRetinopathy2.2. NephropathyNephropathy

3.3. NeuropathyNeuropathyPeripheralPeripheral

Autonomic Autonomic4. Diabetic foot disease4. Diabetic foot disease

MACROVASCULARMACROVASCULAR

1.1. Coronary circulationCoronary circulation

Myocardial ischemia/Myocardial ischemia/infarctioninfarction2.2. Cerebral CirculationCerebral Circulation

TIATIAStrokeStroke

3.3. Peripheral CirculationPeripheral CirculationClaudicationClaudicationIschemiaIschemia


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MACROVASCULARCOMPLICATIONSMACROVASCULARCOMPLICATIONSThe hallmark of diabetic macrovascular disease is accelerated by atherosclerosis involving the aortaThe hallmark of diabetic macrovascular disease is accelerated by atherosclerosis involving the aorta

and large and mediumand large and medium- -sized arteries .sized arteries .C

ard iova scu larC

ard iova scu lar1.1. People with diabetes are 2 to 4 times more likely to develop cardiovascular disease (CVD) thanPeople with diabetes are 2 to 4 times more likely to develop cardiovascular disease (CVD) thanthose without diabetes (more in diabetics with poor glycemic control)those without diabetes (more in diabetics with poor glycemic control)

2.2. Ris k fa c tor s for C HD in Diab e t icsRis k fa c tor s for C HD in Diab e t icslifestyle (eg, cigarette smoking and diet)lifestyle (eg, cigarette smoking and diet)hyperglycemiahyperglycemiahypertensionhypertension

high cholesterolhigh cholesterolinsulin resistanceinsulin resistance

3 .3 . Prevention :Prevention :The American Diabetic Association recommends maintaining an HbA1c level of ,7%, an FPG of The American Diabetic Association recommends maintaining an HbA1c level of ,7%, an FPG of 100 mg/dL, and a glucose level of ,140 mg/dL as determined by OGTT. For this use :100 mg/dL, and a glucose level of ,140 mg/dL as determined by OGTT. For this use :any of the antidiabetic agents including sulfonylureas,meglitinides, biguanides,any of the antidiabetic agents including sulfonylureas,meglitinides, biguanides,

thiazolidinediones, alpha glucosidase inhibitors, and/or insulin.thiazolidinediones, alpha glucosidase inhibitors, and/or insulin. Aspirin at a dose of 81 Aspirin at a dose of 81- -325 mg daily should be added for cardiovascular (CV) protection for325 mg daily should be added for cardiovascular (CV) protection forprimary andprimary and

4.4. S ec ondary pr e ve nt ion:S ec ondary pr e ve nt ion:Maintaining B.P of 130/80 mm Hg in hypertensive diabetics . The antihypertensive agentsMaintaining B.P of 130/80 mm Hg in hypertensive diabetics . The antihypertensive agentsrecommended for treatment include thiazide diuretics, ACE.recommended for treatment include thiazide diuretics, ACE.Inhibitors, ARBs, and nonInhibitors, ARBs, and non- -dihydropyridine calcium channel blockers.dihydropyridine calcium channel blockers.Maintaining LDL 100mg/dl (ideally 70mg/dl), triglycerides 150mg/dL and HDL40mg/dL (men)Maintaining LDL 100mg/dl (ideally 70mg/dl), triglycerides 150mg/dL and HDL40mg/dL (men)and50 mg/dL (women) with use of HMGand50 mg/dL (women) with use of HMG- -CoA reductase inhibitors (statins), bile acid sequestrants,CoA reductase inhibitors (statins), bile acid sequestrants,

fibric acid derivatives, nicotinic acid or cholesterol absorption inhibitorsfibric acid derivatives, nicotinic acid or cholesterol absorption inhibitors


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C e re brova scu larC e re brova scu larThese disorders result from eitherThese disorders result from either

inadequate blood flow to the brain (ie, cerebral ischemia)inadequate blood flow to the brain (ie, cerebral ischemia)hemorrhages into the parenchyma orhemorrhages into the parenchyma orSubarachanoid hemorrhageSubarachanoid hemorrhage

1.1. TI ATI A

in which a patient experiences a temporary focal neurologic deficit such as slurred speech, aphasia, weakness orin which a patient experiences a temporary focal neurologic deficit such as slurred speech, aphasia, weakness orparalysis of a limb, or blindness. These symptoms are rapid in onset,lasting ,24 hours (usually 2 to 15paralysis of a limb, or blindness. These symptoms are rapid in onset,lasting ,24 hours (usually 2 to 15minutes).minutes).

2 . C e re bral infar c t ion2 . C e re bral infar c t ion is a neurologic event causing permanent damage.is a neurologic event causing permanent damage.

3 . C e re bral h em orrhag e3 . C e re bral h em orrhag e is a cerebrovascular disorder that involves escape of blood from blood vessels into theis a cerebrovascular disorder that involves escape of blood from blood vessels into thebrain and its surrounding structures.brain and its surrounding structures.Sudden confusion, loss of coordination, unilateral weakness, and numbness are warning signs of aSudden confusion, loss of coordination, unilateral weakness, and numbness are warning signs of acerebrovascular event.cerebrovascular event.

4. R4. R is k fa c tor s for CV A In Diab e t ics :is k fa c tor s for CV A In Diab e t ics :smokingsmokingobesityobesityhypertensionhypertension

dyslipidemiadyslipidemiatransient ischemic attacks.transient ischemic attacks.

Acu t e tr e at me nt of isc h emic s trok e Acu t e tr e at me nt of isc h emic s trok e

intravenous recombinant tissue plasminogen activator (tPA)intravenous recombinant tissue plasminogen activator (tPA) Aspirin should not be given for the first 24 hours in patients receiving a fibrinolytic agent because doing so Aspirin should not be given for the first 24 hours in patients receiving a fibrinolytic agent because doing sohas been associated with an increased risk of intracranial hemorrhage (ICH) and death.has been associated with an increased risk of intracranial hemorrhage (ICH) and death.

Intra ce re bral Hem orrhag e Manag eme ntIntra ce re bral Hem orrhag e Manag eme nt : : antihypertensive treatment with parenteral agents for systolic pressure higher than 160to 180 mm Hg orantihypertensive treatment with parenteral agents for systolic pressure higher than 160to 180 mm Hg or

diastolic pressures higher than 105 mmHgdiastolic pressures higher than 105 mmHgNitroprusside is the agent most commonly recommended because it can affect a rapid and consistent loweringNitroprusside is the agent most commonly recommended because it can affect a rapid and consistent loweringof the blood pressure to the desired level.of the blood pressure to the desired level.Labetolol is another option.Labetolol is another option.

Seizure prophylaxis (phenytoin 18 mg/kg or fosphenytoin 15 to 20 mg phenytoin equivalent/kg) should beSeizure prophylaxis (phenytoin 18 mg/kg or fosphenytoin 15 to 20 mg phenytoin equivalent/kg) should beconsidered for patients with ICH, especially those with lobar hemorrhage.considered for patients with ICH, especially those with lobar hemorrhage.


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Pe r iph e ral Art e r ial Dise a sePe r iph e ral Art e r ial Dise a se ::1.In diabetes, the risk of PAD is increased by1.In diabetes, the risk of PAD is increased by

Age Ageduration of diabetesduration of diabetespresence of peripheral neuropathy.presence of peripheral neuropathy.

Elevated levels of CElevated levels of C- -reactive protein (CRP),fibrinogenreactive protein (CRP),fibrinogenhomocysteinehomocysteineapolipoprotein Bapolipoprotein B

lipoprotein Alipoprotein Aplasma viscosityplasma viscosity

2. Two2. Two card inal s ym pto ms of P ADcard inal s ym pto ms of P AD areareintermittent claudicationintermittent claudicationpain at rest.pain at rest.Intermittent claudication is characterized by pain, ache, a sense of fatigue, or otherIntermittent claudication is characterized by pain, ache, a sense of fatigue, or other

discomfort that occurs in the affected leg during exercise,particularly walking, and resolvesdiscomfort that occurs in the affected leg during exercise,particularly walking, and resolveswith rest.with rest.Pain at rest occurs in patients with critical limb ischemia in whom the resting metabolic needsPain at rest occurs in patients with critical limb ischemia in whom the resting metabolic needsof the tissue are not adequately met by the available blood supply.of the tissue are not adequately met by the available blood supply.

3. In an effort to manage PAD, practitioners must 3. In an effort to manage PAD, practitioners must

encourage smoking cessationencourage smoking cessationcontrol diabetescontrol diabeteshypertensionhypertensionlipidslipidsphysical activityphysical activityfoot carefoot careinitiate antiplatelet therapy.initiate antiplatelet therapy.

4.Drugs :4.Drugs : FDA has approved 2 drugs, pentoxifylline and cilostazol for treating claudication in patientsFDA has approved 2 drugs, pentoxifylline and cilostazol for treating claudication in patientswith PAD.with PAD.


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MICROVASCULAR COMPLICATIONSMICROVASCULAR COMPLICATIONS

DIABETIC EYE DISEASE: DIABETIC EYE DISEASE: Cataract.Cataract.Diabetic retinopathy.Diabetic retinopathy.

DIABETIC RETINOPATHY DIABETIC RETINOPATHY It is one of the most common causes of blindness inIt is one of the most common causes of blindness inadults between 30 and 65 years of age in developedadults between 30 and 65 years of age in developedcountries.countries.Hyperglycemia increases retinal blood flow and directlyHyperglycemia increases retinal blood flow and directlyaffects retinal endothelial cells and percyte loss,affects retinal endothelial cells and percyte loss,vasoactive substances , endothelial cells proliferation,vasoactive substances , endothelial cells proliferation,capillary closure causing hypoxia leading to VEGFcapillary closure causing hypoxia leading to VEGFproduction leadind to new vasal formation and causingproduction leadind to new vasal formation and causingretinal leakage and exudation.retinal leakage and exudation.


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MANAGEMENT OF DIABETIC EYEMANAGEMENT OF DIABETIC EYE

DISEASEDISEASECataract Extraction : It is indicated if cataract is causing visual disability to the patient or is givingCataract Extraction : It is indicated if cataract is causing visual disability to the patient or is givingrise to inability to view the retina adequately.rise to inability to view the retina adequately.

Good glycemic control particularly in early years reduces risk of diabetic retinopathy.Good glycemic control particularly in early years reduces risk of diabetic retinopathy.

DDCT showed strict glycemic control i.e HbA1c 7% reduced development of retinopathy andDDCT showed strict glycemic control i.e HbA1c 7% reduced development of retinopathy andother microvascular complications by 76%.other microvascular complications by 76%.

Elevated plasma cholesterol is also a risk factor of diabetic retinopathy.Elevated plasma cholesterol is also a risk factor of diabetic retinopathy.

Blood pressure lowering is a proven benefit in hypertension patients.Blood pressure lowering is a proven benefit in hypertension patients.

Regular screening for retinopathy is essential in all dibetics especially those with riskRegular screening for retinopathy is essential in all dibetics especially those with riskfactors (hypertension , use of OCP s , long duration diabetes , pregnancy and evidence of microfactors (hypertension , use of OCP s , long duration diabetes , pregnancy and evidence of microangiopathy as well).The preferred screening option is digital screening photgraphic system withangiopathy as well).The preferred screening option is digital screening photgraphic system with

reference to an opthomogist examination by slit lamp bio microscopyreference to an opthomogist examination by slit lamp bio microscopyNon proliferated and proliferative retinopathy is treated with photo coagulation.Non proliferated and proliferative retinopathy is treated with photo coagulation.

Vitrectomy used in selected cases with advanced diabetic eye disease. Vitrectomy used in selected cases with advanced diabetic eye disease.

Rubeosis iridis is managed by early paRubeosis iridis is managed by early pa- -retinal photo coagulation.retinal photo coagulation.


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Diabetic NephropathyDiabetic NephropathyDiabetic nephropathy is an important cause of morbidity and mortality and is now among theDiabetic nephropathy is an important cause of morbidity and mortality and is now among themost common causes of ESRF in developed countries.most common causes of ESRF in developed countries.

Risk factors for developing diabetic nephropathy are :Risk factors for developing diabetic nephropathy are :1.1. Family history of diabetic nephropathy.Family history of diabetic nephropathy.2.2. Poor control of blood glucose.Poor control of blood glucose.3.3. Long duration of diabetes.Long duration of diabetes.4.4. PrePre--existing hypertension.existing hypertension.

Micro albumin in urea is an important indicator of developing ovrt diabetic nephropathyMicro albumin in urea is an important indicator of developing ovrt diabetic nephropathyespecially in type 1 diabetes.especially in type 1 diabetes.

SC REEN I NG FOR MI C RO ALBU MI N I N UREA :SC REEN I NG FOR MI C RO ALBU MI N I N UREA :

Random urine sample estimate urinary albumin : kretanin ratio (abnormal value : male >2.5Random urine sample estimate urinary albumin : kretanin ratio (abnormal value : male >2.5and female >3.5)and female >3.5)If possible confirm with albumin excretion rate of 30If possible confirm with albumin excretion rate of 30- -300mg /24hrs.300mg /24hrs.Screen type 1 diabetes annually from 5 yrs after diagnosis.Screen type 1 diabetes annually from 5 yrs after diagnosis.Screen type 2 diabetes annually from time of diagnosis.Screen type 2 diabetes annually from time of diagnosis.


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Diabetic Foot Diabetic Foot 1.1. 1010--15% of diabetic15% of diabetic

patient develop diabeticpatient develop diabeticfoot foot

2.2. Factors that combine toFactors that combine toproduce tissue necrosisproduce tissue necrosisto causediabetic foot to causediabetic foot are :are :IschaemiaIschaemiaNeuropathyNeuropathyinfectioninfection

Diabetic foot

Somatic neuropathy :Reduced pain preceptionDecreased proprioception

Clawinfg of toes

Autonomic neuropathyAbsent aweatingDry skin fissures

Reduced bloodflow

Peripheral vascular diseaseClaudication

Cold extremetiesReduced foot pulses


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Management of Diabetic Foot Management of Diabetic Foot

I sc ha emi aI sc ha emi a :ascess blood flow to:ascess blood flow tofeet via doppler ultrasound.feet via doppler ultrasound.Femoral angiography is used toFemoral angiography is used tolocalize area of occlusionlocalize area of occlusionamenable to bypass surgery oramenable to bypass surgery or

angioplastyangioplastyInf ec t ion:Inf ec t ion: Early treatment isEarly treatment isessential with antibiotic .collectionessential with antibiotic .collectionof pus are drained and excision of of pus are drained and excision of infected bone is needed if infected bone is needed if osteomyelitis developosteomyelitis developAvo id pr essu re Avo id pr essu re : insoles and: insoles andspecial shoes must be used tospecial shoes must be used toavoid abnormal pressure over feet avoid abnormal pressure over feet Pat ie nt e d uc at ion:Pat ie nt e d uc at ion: physicianphysician,chirodopodist and surgeon,chirodopodist and surgeon in incollaboration can educate thecollaboration can educate thepatient about foot carepatient about foot care

Distinguishing Features between neuropathy andDistinguishing Features between neuropathy andischaemia in diabetic foot ischaemia in diabetic foot

neuropathyneuropathy ischemiaischemia

symptomsymptom ParesthesiaParesthesiaPainPainnumbnessnumbness

ClaudicationClaudicationRest painRest pain

StructuralStructuraldamagedamage

UlcerUlcerSepsisSepsis

Abcess AbcessOsteomyelitisOsteomyelitisDigitalDigital

gangrenegangreneCharcoat Charcoat

joint joint

UlcerUlcerSepsisSepsisgangrenegangrene


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DIABETIC NEUROPATHY DIABETIC NEUROPATHY Diabetes can damage PNS in aDiabetes can damage PNS in a

number of ways :number of ways : Vascular Hypothesis of Vascular Hypothesis of occlusion of vasa nervorum.occlusion of vasa nervorum.

Hyperglycemia :accumulationHyperglycemia :accumulationof sorbitol and fructose inof sorbitol and fructose inschawnn cell disrupt structureschawnn cell disrupt structureand function.and function.This all leads to :This all leads to :Segmental demyeliation.Segmental demyeliation.

Delayed nerve conductionDelayed nerve conductionvelocity.velocity.Irreversible axonalIrreversible axonaldegeneration.degeneration.

DiabeticDiabeticneuropathy :Histopathologyneuropathy :Histopathology

Axonal degeneration of Axonal degeneration of both myelinated and unboth myelinated and unmyelinated fibres.myelinated fibres.

Thickening of SchwannThickening of Schwanncell basal lamina.cell basal lamina.

Patchy segmentalPatchy segmentaldemyelination.demyelination.

Thickening of basement Thickening of basement

membrane and micromembrane and microthrombi in capillariesthrombi in capillaries

Classification of diabetic neuropathyClassification of diabetic neuropathy

S o m at icS o m at ic

( A)Polyneuropathy( A)Polyneuropathy

1.1. Symmetrical, mainly sensory and distal.Symmetrical, mainly sensory and distal.2.2. Asymmetrical mainly motor amd proximal. Asymmetrical mainly motor amd proximal.(B) Mononeuropathy(B) Mononeuropathy

Au tono mic n eu ropathy Au tono mic n eu ropathy

Gastro IntestinalGastro IntestinalCardio Vascular GenitoUrinaryCardio Vascular GenitoUrinaryGustatoryGustatoryPupillaryPupillarySudomotorSudomotor


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S ymme tr ic al S e n s ory Polyn eu ropathyS ymme tr ic al S e n s ory Polyn eu ropathy Decrease vibratory sensation distally.Decrease vibratory sensation distally.Glove and stocking impairment of other sensations.Glove and stocking impairment of other sensations.Loss of tendon reflexes in lower limb.Loss of tendon reflexes in lower limb.Sensory abnormalities :Sensory abnormalities :

1.1. Paraesthias in feet.Paraesthias in feet.2.2. Pain in lower limbs (especially over shin).Pain in lower limbs (especially over shin).3.3. Burning sensation in soles.Burning sensation in soles.4.4. Numbness in feet.Numbness in feet.5.5. Cutaneous hyperesthesia.Cutaneous hyperesthesia.

Muscle weakness and wasting.Muscle weakness and wasting.Clawed toes.Clawed toes.Foot ulcers and chracot neuroarthropathy.Foot ulcers and chracot neuroarthropathy.

As ymme tr ical m otor n eu ropathy As ymme tr ical m otor n eu ropathy Severe and progressive weakness and wasting of proximal muscle of Severe and progressive weakness and wasting of proximal muscle of lower limb.lower limb.

Severe pain on anterior aspect of leg.Severe pain on anterior aspect of leg.Hyperesthsia and paraesthesia.Hyperesthsia and paraesthesia.Neuropathic CachexiaNeuropathic Cachexia

Mono n eu ropathyMono n eu ropathy 33rdrd and 6and 6 thth cranial nerve palsy.cranial nerve palsy.Carpal tunnel syndrome (median nerve compression).Carpal tunnel syndrome (median nerve compression).Foot drop (Lateral poplital nerve compression).Foot drop (Lateral poplital nerve compression).Truncal radiculopathies.Truncal radiculopathies.

Au tono mic n eu ropathy Au tono mic n eu ropathy CVS: resting tachycardia , postal hypotension, fixed heart rate.CVS: resting tachycardia , postal hypotension, fixed heart rate.GIT: dysphagia ,nocturnal diarrhoea , gastropresis , constepation.GIT: dysphagia ,nocturnal diarrhoea , gastropresis , constepation.GUT: urinary in continence , recurrent infection, ED.GUT: urinary in continence , recurrent infection, ED.Sodomotor : anhydrosis, nocturnal sweats, gastratory sweating.Sodomotor : anhydrosis, nocturnal sweats, gastratory sweating.

Pupillary : decrease or absent light reflex and decreased pupil size.Pupillary : decrease or absent light reflex and decreased pupil size.


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Manag eme nt of Ph e r iph e ral and Au tono mic N eu ropathyManag eme nt of Ph e r iph e ral and Au tono mic N eu ropathyC ond it ionC ond it ion Manag eme ntManag eme nt

Pa in and para es th esi a fro m p e r iph e ral s o m at ic n e ropathyPa in and para es th esi a fro m p e r iph e ral s o m at ic n e ropathy Intensive insulin therapyIntensive insulin therapyTricyclic antiTricyclic anti--depressants.depressants.

Anti convulsants. Anti convulsants.Opiates.Opiates.

Anti Anti--oxidants.oxidants.

Ga s tropar esisGa s tropar esis Dopamine antagonistsDopamine antagonistsErythromycinErythromycin

Po s t u ral Hypot e n si onPo s t u ral Hypot e n si on Support stocking.Support stocking.FludrocortisoneFludrocortisoneNSAIDNSAID

Alpha adren receptor agonist Alpha adren receptor agonist C on s t ipat ionC on s t ipat ion Stimulant laxativeStimulant laxative

Aton ic bladd e r Aton ic bladd e r Intermittent self catheterization.Intermittent self catheterization.

Ex cessi ve s w e at ingEx cessi ve s w e at ing ClonidineClonidine Anti Anti--cholinergic drugs.cholinergic drugs.Topical anti muscrinic agent.Topical anti muscrinic agent.

Diarrh e aDiarrh e a LoperamideLoperamide Antibiotics AntibioticsChlonidineChlonidineOcteroitideOcteroitide

Erec t ile Dys fu n c t ionErec t ile Dys fu n c t ion Phophodiesterase type 5 inhibitors (sidenafil)Phophodiesterase type 5 inhibitors (sidenafil)----oraloralDopamine agonist Dopamine agonist- -sublingualsublingualProsatgladin E1Prosatgladin E1 injected into corpus cavernosuminjected into corpus cavernosum

Vacuum tumescence devices. Vacuum tumescence devices.Implanted penile prosthesis.Implanted penile prosthesis.Psychological counselling.Psychological counselling.


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Diabetic EmergenciesDiabetic EmergenciesDiab e t ic Ke toa ci do sisDiab e t ic Ke toa ci do sis

Introd uc t ion:Introd uc t ion:Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated withDiabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated withhigh blood levels of sugar level and organic acids called ketones.high blood levels of sugar level and organic acids called ketones.occurs mostly in type 1 ( juvenile) diabetes mellitus (T1DM)occurs mostly in type 1 ( juvenile) diabetes mellitus (T1DM)Males and females are equally affected.Males and females are equally affected.

Pr eci p itat ing fa c tor sPr eci p itat ing fa c tor sdehydrationdehydration

infection such as diarrhea, vomiting, and/or high fever (40%),infection such as diarrhea, vomiting, and/or high fever (40%),missed or inadequate insulin (25%), andmissed or inadequate insulin (25%), andnewly diagnosed or previously unknown diabetes (15%).newly diagnosed or previously unknown diabetes (15%).

Various other causes may include a heart attack, stroke, trauma, stress, alcohol abuse, drug abuse, and surgery. Various other causes may include a heart attack, stroke, trauma, stress, alcohol abuse, drug abuse, and surgery. Approximately 5% to 10% of cases have no identifiable cause. Approximately 5% to 10% of cases have no identifiable cause.

Diab e t ic Ke toa ci do sis S ym pto msDiab e t ic Ke toa ci do sis S ym pto ms

A p e rs on d e ve lop ing d iab e t ic ke toa cido sis m ay hav e on e or m or e of th ese s ym pto ms : A p e rs on d e ve lop ing d iab e t ic ke toa cido sis m ay hav e on e or m or e of th ese s ym pto ms :Poly u r ia , polyd ip si aPoly u r ia , polyd ip si ag e n e ral w e akn ess ,g e n e ral w e akn ess ,vo mi t ingvo mi t inglo ss of app e t it e ,lo ss of app e t it e ,conf usi on,conf usi on,abdo mi nal pa inabdo mi nal pa ins hortn ess of br e ath,s hortn ess of br e ath,dry s k in,dry s k in,dry m o u th,dry m o u th,Hypot e n si onHypot e n si onta chy card iata chy card iaTa chypn e a,ka ss a m a u l br e ath indTa chypn e a,ka ss a m a u l br e ath inda d is t in c t ive fr ui ty odor on th e br e atha d is t in c t ive fr ui ty odor on th e br e ath


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Management Of DiabeticManagement Of Diabetic

KetoacidosisKetoacidosisEx a ms and T es t sEx a ms and T es t sBlood tests for : levels of sugar, potassium, sodium, and other electrolytes. Ketone level ,RFT s and ABG sBlood tests for : levels of sugar, potassium, sodium, and other electrolytes. Ketone level ,RFT s and ABG sOther tests to know underlying factor : chest X Other tests to know underlying factor : chest X--ray, electrocardiogram ECG, urine analysis, and possibly a CT scan of the brain.ray, electrocardiogram ECG, urine analysis, and possibly a CT scan of the brain.

Me d ical Tr e at me ntMe d ical Tr e at me ntFluid replacement and insulin administration intravenously (IV)Fluid replacement and insulin administration intravenously (IV) are the primary and most critical initial treatments toare the primary and most critical initial treatments to

1.1. reverse dehydrationreverse dehydration2.2. lower blood acid levelslower blood acid levels3.3. restore normal sugar and electrolyte balance.restore normal sugar and electrolyte balance.

Pha se 1 of m anag eme nt:Pha se 1 of m anag eme nt: Admission to ICU Admission to ICUInsulin 6units/hour by I/V infusion or 20units I/M stat followed by 6units I?M hourlyInsulin 6units/hour by I/V infusion or 20units I/M stat followed by 6units I?M hourlyFluid replacement : 0.9%NaCl with 20mmol KCL /liter . Average regime is 1L in 30min and next 1L in 1hour and next 1L in 2hourFluid replacement : 0.9%NaCl with 20mmol KCL /liter . Average regime is 1L in 30min and next 1L in 1hour and next 1L in 2hours t s thenhen1L in 4hours then 1L in 6hours1L in 4hours then 1L in 6hours

Adjust KCl concentration on 2hourly blood Klevel Adjust KCl concentration on 2hourly blood KlevelBlood pressure below 80mm of Hg gives plasma expanderBlood pressure below 80mm of Hg gives plasma expanderPh below 7 gives 500ml of sodium bicarbonate 1.26%+ 10 milli mole KClPh below 7 gives 500ml of sodium bicarbonate 1.26%+ 10 milli mole KCl

Pha se 2 m anag eme ntPha se 2 m anag eme ntWhen blood glucose falls to 10When blood glucose falls to 10- -12 millimole per litre change infusion fluid to 1 litre 5% dextrose + 20millimole KCl hourly.Cont 12 millimole per litre change infusion fluid to 1 litre 5% dextrose + 20millimole KCl hourly.Continue inueinsulin with dose adjusted according to hourly blood glucose test result (insulin with dose adjusted according to hourly blood glucose test result ( 3 units per hour when glucose 15millimole per litre).3 units per hour when glucose 15millimole per litre).

PH AS E 3 M ANAGE MEN TPH AS E 3 M ANAGE MEN TOnce stable and able to eat and drink normally transfer patient to (4 times)daily subcutaneous insulin regime.Once stable and able to eat and drink normally transfer patient to (4 times)daily subcutaneous insulin regime.SPECIAL MEASURESSPECIAL MEASURESBroad spectrum antibiotic if infection is likelyBroad spectrum antibiotic if infection is likelyNG tube if drowsyNG tube if drowsyConsider CVP pressure monitoring if patient is shocked or has cardiac or renal impairment.Consider CVP pressure monitoring if patient is shocked or has cardiac or renal impairment.Bladder Cathater if no urine passed in 2 hrs.Bladder Cathater if no urine passed in 2 hrs.S UB S EQUEN T M ANAGE MEN TS UB S EQUEN T M ANAGE MEN TMonitor glucose hourly 4 8 hrs.Monitor glucose hourly 4 8 hrs.Monitor electrolytes 2 hourly for 8 hours.Monitor electrolytes 2 hourly for 8 hours.

Adjust potassium according to results. Adjust potassium according to results.


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PreventionPrevention

Actions a person with diabetes can take to prevent diabetic ketoacidosis Actions a person with diabetes can take to prevent diabetic ketoacidosisinclude :include :close monitoring and control of blood sugars, especially during times of close monitoring and control of blood sugars, especially during times of infection, stress, trauma, or other serious illness;infection, stress, trauma, or other serious illness;taking extra insulin injections or other diabetes medications on time astaking extra insulin injections or other diabetes medications on time asdirected by your health care practitioner; anddirected by your health care practitioner; andcontacting health care practitioner or seeking medical attention promptly ascontacting health care practitioner or seeking medical attention promptly asneeded.needed.With aggressive treatment, most people who develop diabetic ketoacidosisWith aggressive treatment, most people who develop diabetic ketoacidosiscan expect complete recovery. Death is rare (2% of cases), but can occurcan expect complete recovery. Death is rare (2% of cases), but can occurwhen the condition is not treated.when the condition is not treated.C

o m pl ic at ion s :C

o m pl ic at ion s :C o m pl ic at ion s fro m tr e at me ntC o m pl ic at ion s fro m tr e at me nt of diabetic ketoacidosis include low bloodof diabetic ketoacidosis include low bloodsugar, low potassium, pulmonary edema, seizure, cardiorespiratory arrest,sugar, low potassium, pulmonary edema, seizure, cardiorespiratory arrest,or swelling of the brain (cerebral edema).or swelling of the brain (cerebral edema).Complications are also possible from associated illnesses such as infection,Complications are also possible from associated illnesses such as infection,stroke, and heart attacks.stroke, and heart attacks.


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Hperosmolar N0nHperosmolar N0n- -Ketotic DiabeticKetotic Diabetic

ComaComaEtiology :Etiology :Dehydration syndrome due to hyperglycaemiaDehydration syndrome due to hyperglycaemiaDue to insufficient insulin to prevent hyperglycaemia but enough to prevent significant ketoacidosisDue to insufficient insulin to prevent hyperglycaemia but enough to prevent significant ketoacidosisOften develops during severe illness or physiologic stress in elderly patients either with no history of diabetes or with aOften develops during severe illness or physiologic stress in elderly patients either with no history of diabetes or with a hi history of story of

NIDDMNIDDM

DI AGN OS I SDI AGN OS I SUndiagnosed Type 2 DM or known cases of Type 2 DMUndiagnosed Type 2 DM or known cases of Type 2 DMHyperglycaemia (blood glucose often > 28 mmol/l)Hyperglycaemia (blood glucose often > 28 mmol/l)Usually no ketones in the urine, although may be present in patient withUsually no ketones in the urine, although may be present in patient with

vomiting ( Particularly trace or 1+)vomiting ( Particularly trace or 1+)No severe acidosis (pH >7.2 and HCO3No severe acidosis (pH >7.2 and HCO3

-- often normal)often normal)Hyperosmolality (serum osmolality >350 mosm/l)Hyperosmolality (serum osmolality >350 mosm/l)50% of patients are hypernatraemic50% of patients are hypernatraemic

decreased conscious level and mental confusiondecreased conscious level and mental confusion

PR EC IPIT ATI NG E VEN TPR EC IPIT ATI NG E VEN TIn elderly patients, consider MI, chest infection, etcIn elderly patients, consider MI, chest infection, etcUsually underlying infection (URTI, diarrhoea and vomiting, UTI, etc, while tempUsually underlying infection (URTI, diarrhoea and vomiting, UTI, etc, while temp

and WCC unhelpful)and WCC unhelpful)Newly presenting patient Newly presenting patient Acute abdomenAcute abdomen

I N ITI AL I N VES TI GA TIO N SI N ITI AL I N VES TI GA TIO N SGlucoseGlucoseSerum electrolytesSerum electrolytesInfection screen (including CXR and blood cultures)Infection screen (including CXR and blood cultures)Arterial blood gasesArterial blood gasesCalculation of serum osmolality {= 2 (K+ + Na+ ) + urea + glucose (all in mmol/l)},Calculation of serum osmolality {= 2 (K+ + Na+ ) + urea + glucose (all in mmol/l)},

and measurement by the laboratoryand measurement by the laboratoryUrinalysis and ECGUrinalysis and ECG


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Clinical Features :Clinical Features :C lin ic al F e at u resC lin ic al F e at u res

Typical patient is an elderly nursing home resident Typical patient is an elderly nursing home resident ConstitutionalConstitutional malaise, weakness, myalgiamalaise, weakness, myalgiaAbdominal pain, nausea and vomitingAbdominal pain, nausea and vomitingPolyuria, polydipsia and loss of weight Polyuria, polydipsia and loss of weight Signs of volume depletion and hypoperfusion +/Signs of volume depletion and hypoperfusion +/- - hypovolaemic shockhypovolaemic shockHyperventilation Kussmaul s breathing in severe acidosis), ketotic breath, pyrexiaHyperventilation Kussmaul s breathing in severe acidosis), ketotic breath, pyrexiaPyrexiaPyrexiaSeizures or focal neurologic signs, stupor, comaSeizures or focal neurologic signs, stupor, comaEvidence of precipitating causesEvidence of precipitating causes

o Sepsis eg UTI, respiratory tract infection, bacterial meningitis, retropharyngeal abscess,o Sepsis eg UTI, respiratory tract infection, bacterial meningitis, retropharyngeal abscess,hepatobiliary sepsis. Examine for sources of sepsis include hidden sites eg scalp, back, auditoryhepatobiliary sepsis. Examine for sources of sepsis include hidden sites eg scalp, back, auditorymeatus, perianal regionmeatus, perianal regiono Noncompliance with diet or insulin therapyo Noncompliance with diet or insulin therapyo Traumao Traumao AMIo AMIo CVAo CVAo Pancreatitiso Pancreatitiso Parenteral glucose admin, TPNo Parenteral glucose admin, TPNo Drugs : glucocorticoids, thiazides, phenytoin,o Drugs : glucocorticoids, thiazides, phenytoin, --blockers, calcium channel blockersblockers, calcium channel blockers


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Management Of HONK Management Of HONK Pr in cipl es of Manag eme ntPr in cipl es of Manag eme nt1. Aggressive fluid management 1. Aggressive fluid management 2. IV soluble insulin2. IV soluble insulin3. Aggressive K replacement except in renal failure3. Aggressive K replacement except in renal failure4. Look for precipitating factors4. Look for precipitating factorsTr eatment Tr eatment Flui d t h e r a pyFlui d t h e r a pyAggressive fluid replacement about 2 L in 4 h, 1Aggressive fluid replacement about 2 L in 4 h, 1- -2 L in the next 4 h; about 42 L in the next 4 h; about 4- -7 L in total within the first 24 h7 L in total within the first 24 hNS is preferred because it helps to maintain intravascular volume and maintain peripheral perfusion. It may also reduce risNS is preferred because it helps to maintain intravascular volume and maintain peripheral perfusion. It may also reduce risk o k of cerebralf cerebral

oedema when sugar is loweredoedema when sugar is lowered NS is used if serum Na >150 NS is used if serum Na >150- -155mmol/L155mmol/LChange to D5% with additional NaCl when blood sugar is 70kgIn severely insulin resistant cases eg morbid obesity, severe sepsis, high dose glucocorticoid treatment and TPN, a slidingIn severely insulin resistant cases eg morbid obesity, severe sepsis, high dose glucocorticoid treatment and TPN, a sliding sc scale with anale with an

initial rate of >10/h may be requiredinitial rate of >10/h may be required

Pota ssium re pla ceme ntPota ssium re pla ceme ntAggressive IV K+ infusion should be given in initial phase because of the shift of K+ with glucose into the intracellular cAggressive IV K+ infusion should be given in initial phase because of the shift of K+ with glucose into the intracellular comp ompartment artment

with hydration and insulin treatment with hydration and insulin treatment In presence of ECG changes of hypokalaemia, 30 mmol of K+ diluted in 1 litre NS or NS should be given over 1 h before labIn presence of ECG changes of hypokalaemia, 30 mmol of K+ diluted in 1 litre NS or NS should be given over 1 h before labora oratorytory

confirmation is available.confirmation is available.Review K+ infusion rate when blood sugar is normalizing (


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Hypoglycemia In Diabetics :Hypoglycemia In Diabetics :Fa c tor s le ad ing to hypogly cemi a in d iab e t es :Fa c tor s le ad ing to hypogly cemi a in d iab e t es :

After a meal with a lot of simple sugars called as reactive hypoglycemia. After a meal with a lot of simple sugars called as reactive hypoglycemia.Missing a mealMissing a mealDelaying mealDelaying mealdoesn't eat when illdoesn't eat when illdrinks alcohol wihout eating any food.drinks alcohol wihout eating any food..Intense exercise may also trigger a hypoglycemic reaction..Intense exercise may also trigger a hypoglycemic reaction.Diab e t es Dru g s Link e d to Hypogly cemi aDiab e t es Dru g s Link e d to Hypogly cemi aThese include the sulfonylureas and meglitinides.These include the sulfonylureas and meglitinides.

Alpha Alpha--glucosidase inhibitors, biguanides, and thiazolidinediones alone should not cause hypoglycemia but can when used with otheglucosidase inhibitors, biguanides, and thiazolidinediones alone should not cause hypoglycemia but can when used with other rdiabetes medicines.diabetes medicines.The older oral diabetic medications tend to cause low sugar more frequently than newer drugs used to t reat type 2 diabetes. EThe older oral diabetic medications tend to cause low sugar more frequently than newer drugs used to t reat type 2 diabetes. Exam xamplesplesof these first generation drugs include :of these first generation drugs include :tolbutamide,Tolinase tolazamide),chlorpropamidetolbutamide,Tolinase tolazamide),chlorpropamide

Other drugs that can cause low blood sugars inlude the use of alcohol, aspirin,warfarin, allopurinol, probenecid with diabetiOther drugs that can cause low blood sugars inlude the use of alcohol, aspirin,warfarin, allopurinol, probenecid with diabetic cmedications.medications.Excess insulin intakeExcess insulin intake

S ym pto ms of Hypogly cemi aS ym pto ms of Hypogly cemi a These signs or symptoms usually include altered mental status and/or sympathetic nervous systemThese signs or symptoms usually include altered mental status and/or sympathetic nervous systemstimulation. The glucose level at which an individual becomes symptomatic is highly variable.stimulation. The glucose level at which an individual becomes symptomatic is highly variable.Most people feel symptoms of hypoglycemia when their blood sugar is 70 mg/dL or lower.Most people feel symptoms of hypoglycemia when their blood sugar is 70 mg/dL or lower.Each person with diabetes may have different symptoms of hypoglycemia.Each person with diabetes may have different symptoms of hypoglycemia.Early symptoms of hypoglycemia may include :Early symptoms of hypoglycemia may include :ConfusionConfusionDizzinessDizzinessHungerHungerHeadachesHeadachesIrritabilityIrritabilityPalpatationsPalpatationsPale skinPale skinSweatingSweatingTremblingTremblingWeaknessWeakness

Anxiety Without treatment, more severe hypoglycemia symptoms may develop, including : Anxiety Without treatment, more severe hypoglycemia symptoms may develop, including :HeadacheHeadacheFeeling irritableFeeling irritablePoor coordination and concentrationPoor coordination and concentrationNumbness in mouth and tongueNumbness in mouth and tongueComaComa


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Managememnt and Prevention Of Managememnt and Prevention Of Hypoglycemia In Diabetics :Hypoglycemia In Diabetics :

Hypogly cemi a Tr e at me nt in Diab e t esHypogly cemi a Tr e at me nt in Diab e t es

Eme rg e n cy De part me nt

Car e

Eme rg e n cy De part me nt

Car eThe initial approach should include the following :The initial approach should include the following :

ABCs, intravenous (IV) access, oxygen, monitoring, and Accucheck. ABCs, intravenous (IV) access, oxygen, monitoring, and Accucheck. Administration of glucose as part of the initial evaluation of altered mental status often corrects hypoglycemia. Administration of glucose as part of the initial evaluation of altered mental status often corrects hypoglycemia.

As was the case in the field, treatment should not be withheld while waiting for a laboratory glucose value. Because the brai As was the case in the field, treatment should not be withheld while waiting for a laboratory glucose value. Because the brain u n usessesglucose as its primary energy source, neuronal damage may occur if treatment of hypoglycemia is delayed.glucose as its primary energy source, neuronal damage may occur if treatment of hypoglycemia is delayed.

A hyperglycemic patient with an altered mental status may receive a bolus of glucose. This procedure is unlikely to harm the A hyperglycemic patient with an altered mental status may receive a bolus of glucose. This procedure is unlikely to harm thepatient with high glucose; however, the delay in giving glucose to the hypoglycemic patient may be detrimental.patient with high glucose; however, the delay in giving glucose to the hypoglycemic patient may be detrimental.

If an Accucheck can be performed immediately, awaiting the results of this test (available within 1 minute) before decidingIf an Accucheck can be performed immediately, awaiting the results of this test (available within 1 minute) before decidingwhether to administer glucose is reasonable.whether to administer glucose is reasonable.

Once the diagnosis of hypoglycemia is made, search carefully for the cause in the previously healthy patient.Once the diagnosis of hypoglycemia is made, search carefully for the cause in the previously healthy patient.In the diabetic patient, search diligently for the cause (eg, medication changes, dietary changes, new metabolic changes, recIn the diabetic patient, search diligently for the cause (eg, medication changes, dietary changes, new metabolic changes, recent ent illness,illness,

occult infection) of the episode.occult infection) of the episode.M edication M edication

The mainstay of therapy for hypoglycemia is glucose. Other medications may be administered based on the underlying cause or t The mainstay of therapy for hypoglycemia is glucose. Other medications may be administered based on the underlying cause or the heaccompanying symptoms; however, these medications are not addressed in this article.accompanying symptoms; however, these medications are not addressed in this article.G luc o se su ppl eme ntG luc o se su ppl eme ntThis agent is used to raise the patient's serum glucose.This agent is used to raise the patient's serum glucose.De x tro se ( G luc oseDe x tro se ( G luc ose--D)D)Monosaccharide absorbed from intestine and distributed, stored, and used by tissues. Parenterally injected dextrose is used iMonosaccharide absorbed from intestine and distributed, stored, and used by tissues. Parenterally injected dextrose is used in p n patientsatientsunable to obtain adequate oral intake. Direct oral absorption results in rapid increase of blood glucose concentrations.unable to obtain adequate oral intake. Direct oral absorption results in rapid increase of blood glucose concentrations.Effective in small dosesEffective in small dosesno evidence that it may cause toxicit no evidence that it may cause toxicit Concentrated dextrose infusions provide higher amounts of glucose and increased caloric intake with minimum fluid volume.Concentrated dextrose infusions provide higher amounts of glucose and increased caloric intake with minimum fluid volume.

C hang eC hang e in dose of insulin can also help overcome hypoglycemiain dose of insulin can also help overcome hypoglycemia

Hypogly cemi a Pr e ve nt ion for Tho se W ith Di ab e t esHypogly cemi a Pr e ve nt ion for Tho se W ith Di ab e t esProper meal plan.Proper meal plan.Eat at least three evenly spaced meals each day with betweenEat at least three evenly spaced meals each day with between- -meal snacks as prescribed.meal snacks as prescribed.Plan your meals no more than four to five hours apart.Plan your meals no more than four to five hours apart.Exercise 1/2 to one hour after meals.Exercise 1/2 to one hour after meals.DoubleDouble--check insulin and dose of diabetes medicine before taking it check insulin and dose of diabetes medicine before taking it

Being able recognize the warning signs of low blood sugar and treat it promptly.Being able recognize the warning signs of low blood sugar and treat it promptly.Carrying enenrgy rich snackCarrying enenrgy rich snackSession with health care provider in case of frequent hypoglycemic episodes.Session with health care provider in case of frequent hypoglycemic episodes.


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Diabetic Complications and Emergencies

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