chronic kidney disease complications

7/24/2019 Chronic Kidney Disease Complications

1/18

2014

COMPLICATIONS of CKD

Secondary to

Diabetic Nephropathy

Need for DialyMirasol, Jaso

Diabe

NeuropathMirasol, Jaso

Diabe

RetinopathAntonio, Neil Bria

Diabetic Vascul

DiseaBerco, Arly

Coronary Arte

DiseaOrcini, V

Hyperglycem

Hyperosmol

StaPadrinao, Jimm

In Partial Fulfilment

of the Requirements

for Nephrology

Submitted to:

Dr. R. Valenzona


2/18

The kidneys function to remove waste products from the blood. Sometimes this filtering system breaks

down. Diabetes can damage the kidneys and cause them to fail. Failing kidneys lose their ability to filter

out waste products, resulting in kidney disease. High levels of blood sugar make the kidneys filter too

much blood. All this extra work is hard on the filters. After many years, they start to leak and useful

protein is lost in the urine.

In time, the stress of overwork causes the kidneys to lose their filtering ability. Waste products then

start to build up in the blood. Finally, the kidneys fail. This failure, ESRD, is very serious. A person with

ESRD needs to have a kidney transplant or to undergo dialysis.

Diabetic neuropathy is a peripheral nerve disorder caused by diabetes or poor blood sugar control. The

most common types of diabetic neuropathy result in problems with sensation in the feet. It can develop

slowly after many years of diabetes or may occur early in the disease. The symptoms are numbness,

pain, or tingling in the feet or lower legs. The pain can be intense and require treatment to relieve the

discomfort. The loss of sensation in the feet may also increase the possibility that foot injuries will go

unnoticed and develop into ulcers or lesions that become infected. In some cases, diabetic neuropathy

can be associated with difficulty walking and some weakness in the foot muscles. There are other types

of diabetic-related neuropathies that affect specific parts of the body. For example, diabetic amyotrophy

causes pain, weakness and wasting of the thigh muscles, or cranial nerve infarcts that may result in

double vision, a drooping eyelid, or dizziness. Diabetes can also affect the autonomic nerves that control

blood pressure, the digestive tract, bladder function, and sexual organs. Problems with the autonomic

nerves may cause lightheadedness, indigestion, diarrhea or constipation, difficulty with bladder control,

and impotence.

Parameters Characteristics of DM Neuropathy Case

Epidemiology Most common complication of

diabetes mellitus

DM affects men and women with

equal frequency.

can occur at any age but is more

common with increasing age and

severity and duration of diabetes.

The patient is diabetic

Female

57 years old

Need forDialysisby: Jason M. Mirasol

DiabeticNeuropathyby: Jason M. Mirasol


3/18

Risk Factors Poor glycemic control

Advanced age

Long duration of DM

Hypertension

Uncontrolled diabetes

Advanced age

Long standing DM

Uncontrolled

hypertension

Clinical Manifestations

History

Sensory manifestations

Motor manifestations

Physical Examination

Sensory

deep tendon reflexes

Motor

feelings of numbness or deadness

of both legs and feet

proximal and distal weakness of

the lower extremities

decrease or loss of vibratory and

pinprick sensation over the toes

commonly hypoactive or absent.

proximal and distal weakness of

the lower extremities

Patient cannot feel her

legs and feet

Patients legs and feet are

weak.

Patient cannot detect the

vibrations from the tuning

fork or distinguish dull or

sharp.

DTRs are not elicited

Patient cannot move her

lower extremities

Discussion

Neuropathies are the most common complication of diabetes mellitus (DM), affecting up to 50% of

patients with type 1 and type 2 DM. Patients with type 2 diabetes mellitus may present with distalpolyneuropathy after only a few years of known poor glycemic control; sometimes, these patients

already have neuropathy at the time of diagnosis.

In our case, the patient has no strict compliance to her anti-hyperglycemic medications. Consequently,

the above symptoms were noted together with a group of comorbid conditions. And because of her

many risk factors, it is more probable for her to manifest with such complications.

Pathophysiology

Hyperglycemia causes increased levels of intracellular glucose in nerves, leading to saturation of the

normal glycolytic pathway. Extra glucose is shunted into the polyol pathway and converted to sorbitol

and fructose by the enzymes aldose reductase and sorbitol dehydrogenase.Accumulation of sorbitol and

fructose lead to reduced nerve myoinositol, decreased membrane Na+/K+ -ATPase activity, impaired

axonal transport, and structural breakdown of nerves, causing abnormal action potential propagation.

This is the rationale for the use of aldose reductase inhibitors to improve nerve conduction.


4/18

Complications of Diabetic Neuropathy

Once the patient has develop diabetic neuropathy, clinicians should be very cautious because this can

cause a number of more serious complications, including:

1.

Loss of a limb-Because nerve damage can cause a lack of feeling in your feet, cuts and soresmay go unnoticed and eventually become severely infected or ulcerated a condition in which

the skin and soft tissues break down. The risk of infection is high because diabetes reduces

blood flow to your feet.

Infections that spread to the bone and cause tissue death (gangrene) may be impossible to treat

and require amputation of a toe, foot or even the lower leg.

2. Charcot joint- This occurs when a joint, usually in the foot, deteriorates because of nerve

damage. Charcot joint is marked by loss of sensation, as well as swelling, instability and

sometimes deformity in the joint itself.

3.

Urinary tract infections and urinary incontinence- Damage to the nerves that control your

bladder can prevent it from emptying completely. This allows bacteria to multiply in your

bladder and kidneys, leading to urinary tract infections. Nerve damage can also affect your

ability to feel when you need to urinate or to control the muscles that release urine.

4. Low blood pressure-Damage to the nerves that control circulation can affect your body's ability

to adjust blood pressure. This can cause a sharp drop in pressure when you stand after sitting

(orthostatic hypotension), which may lead to dizziness and fainting.

Treatment

The goal of treating diabetic neuropathy is to prevent further tissue damage and relieve discomfort. The

first step is to bring blood sugar levels under control by diet and medication. Another important part of

treatment involves taking special care of the feet by wearing proper fitting shoes and routinely checking

the feet for cuts and infections. Analgesics, low doses of antidepressants, and some anticonvulsant

medications may be prescribed for relief of pain, burning, or tingling. Some individuals find that walking

regularly, taking warm baths, or using elastic stockings may help relieve leg pain.

Prognosis

The prognosis for diabetic neuropathy depends largely on how well the underlying condition of diabetes

is handled. Treating diabetes may halt progression and improve symptoms of the neuropathy, butrecovery is slow. The painful sensations of diabetic neuropathy may become severe enough to cause

depression in some patients.


5/18

References:

Carrington AL, Litchfield JE. The aldose reductase pathway and nonenzymatic glycation in the

pathogenesis of diabetic neuropathy: a critical review for the end of the 20th century. Diabetes

Reviews. 1999.;7:275-99.

Greene DA, Arezzo JC, Brown MB. Effect of aldose reductase inhibition on nerve conduction and

morphometry in diabetic neuropathy. Zenarestat Study Group. Neurology. Aug 11 1999;53(3):580-91.

American Academy of Neurology; Diabetic Neuropathy; American Brain Foundation;

http://patients.aan.com/disorders/index.cfm?event=view&disorder_id=907

American Diabetes Association; How Does Diabetes Cause Kidney Disease?; Diabetes Forecast

Magazine; December 10, 2013; http://www.diabetes.org/living-with-diabetes/complications/kidney-

disease-nephropathy.html

Matured Cataract, Diabetic & Hypertensive Retinopathy

Patient M.A. was diagnosed with Diabetes Mellitus type II since 1990 and hypertensive since1995 with peak blood pressure of 160/100 (Stage 2 hypertension, JNC 7); usual blood pressure of

150/90 (stage 1 hypertension, JNC7) with maintenance medication since then, however, with missed

medication that was claimed to be 2 days weekly. Even though with medication and on good

compliance, due to 24 years DM and 19 years HTN stage II (JNC VII), the patient was expected to have

diabetic and hypertensive retinopathy as well as cataract secondary to long standing diabetic

retinopathy. Patient claims gradual blurring of vision on both eyes since 2009 and was prescribed with

Trimetazide dihydrochloride (Vastarel 20) 20 mg tablet for thrice daily after meal with poor compliance

and no improvement on vision of both eyes. During fundoscopic examination of the patient, both ROR

shows negative result due to mature cataract on presentation, however, we could not totally rule out

the possibilities of pathology in the retina and highly considered it since the patient has high risk unless

and we can only visualized the retina after phacoemulsification surgery has been done. Diabeticretinopathy and Hypertensive retinopathy that may be part of the complication of the patient may be

asymptomatic at initial presentation, but the manifestation of retinal disease may be masked by the lens

problem which is matured cataract secondary to diabetes mellitus.

DiabeticRetinopathyby: Neil Brian B. Antonio


6/18

Patient MA Cataract in DM Diabetic Retinopathy Hypertensive

Retinopathy

Epidemiology in

Philippines

Diagnosed DM II (24

years), Stage II HTN (JNC

VII) (19 years) , resides in

Bian, Laguna which may

be part of 24% shown in

studies with DM

retinopathy in Luzon other

than Metro, Manila with

34% in Study by Diabetes

Center of the Philippines

August 30, 20141

57 year-old

(19961998)a total of

1269 diabetics from 45

hospitals and diabetes

clinics nationwide

were screened by

ophthalmologists for

cataract and diabetic

retinopathy using

fundoscopic

examination

fundoscopic tests, 49%

had abnormal eye

findings; 28% with

diabetic retinopathy

(DR); and 28% with

cataract

2-fold in 5-year

incidence of cortical

cataract in Impaired

Fasting Glucose (IFG)2

Incident posterior

subcapsular (PSC)

cataract was more

frequent among

persons with diabetes2

3-4x cataract

prevalaence with DM

under the age of 65

which may be

applicable to our

patient at 57 year-old

and with 2x excess

prevalence beyond 65year-old and the most

frequently seen type of

cataract is age-related

or senile cataract

which tends to occur

earlier and progress

more rapidly than

nondiabetic patient3

fundoscopic tests,

49% had abnormal

eye findings; 28%

with diabetic

retinopathy (DR);

Out of 28% with DR

22% were in the

background stage,

6% were in

preproliferative and

proliferative stages1

No data available

HPI with gradual BOV, O.U.

since 2009

with gradual blurring

of vision usually both

eyes

with gradual

blurring of vision

usually both eyes,

but may also be

sudden if present

with active bleedingor vitreous

hemorrhage

with gradual

blurring of vision

usually both eyes

Physical

Examination

160/90mmHg (right arm

supine); peak BP of

160/100 (Stage 2

hypertension, JNC 7);

usual BP of 150/90 (stage

1 hypertension, JNC7)

with maintenance

pupils are usually mid

dilated 4-5 mm equally

non-reactive to light;

patient may see

clearer on peripheral

vision in nuclear

cataract making visual

pupils are usually 3-

4 mm equally

equally reactive to

light in the absence

of cataract or

pathology that

visual acuity

pupils are usually

3-4 mm equally

equally reactive to

light in the absence

of cataract or

pathology that

visual acuity


7/18

medication

Pupils are round measuring

mm, symmetrical, both non

reactive to light. Intact V

and intact EOM

Visual acuity 20/400 o

both eyes

Fundoscopic : No ROR, haz

media on both eyes

field intact but

decreased

VA usually decreased

depending on type of

cataract and maturity

of cataract

mature cataract will

obscured light flow

directly to retina

showing dark or hazy

media

VA usually to

20/200 or more

DM retinopathy in

the absence of

cataract in early

stage may show

ROR since no

obstruction of light

towards the

vascular choroid

passing through

transparent retina

but may show

sudden BOV once

positive vitreous

hemorrhage

VA usually to

20/200 or more

Hypertensive

retinopathy in the

absence of cataract

in early stage may

show ROR since no

obstruction of light

towards the

vascular choroid

passing through

transparent retina

but may suddenly

decreased if

positive ruptured

blood vessels

References:

1. Diabetic Retinopaties in Filipinos, Philippine Center for Diabetes Education issued last August 30, 2014;

http://www.diabetescenter.org.ph/

2. http://www.ncbi.nlm.nih.gov/pubmed/15512989

3. Journal of Ophthalmology: Diabetic Cataract, Article ID 608751, Schmidt-Erfurth, et. al., 2010

Pathophysiology of DM Retinopathy
http://www.ncbi.nlm.nih.gov/pubmed/15512989http://www.ncbi.nlm.nih.gov/pubmed/15512989


8/18

Actually, the exact mechanism by which diabetes causes retinopathy remains unclear, but

several theories have been postulated to explain the typical course and history of the disease. Growth

hormone in the form of VEGF; platelet and blood viscosity; aldose reductase and vasoproliferative

factors may contribute to the pathophysiology. Growth hormone appears to cause the development andprogression of diabetic retinopathy. While increased erythrocyte aggregation, decreased red blood cell

deformability, increased platelet aggregation, and adhesion, predispose the patient to sluggish

circulation, endothelial damage, and focal capillary occlusion leads to retinal ischemia, which, in turn,

contributes to the development of diabetic retinopathy. Increased levels of blood glucose are thought to

have a structural and physiologic effect on retinal capillaries causing them to be both functionally and

anatomically incompetent. A persistent increase in blood glucose levels shunts excess glucose into the

aldose reductase pathway in certain tissues, which converts sugars into alcohol like glucose into sorbitol,

galactose to dulcitol. Intramural pericytes of retinal capillaries seem to be affected by this increased

level of sorbitol, eventually leading to the loss of their primary function like autoregulation of retinal

capillaries. Resulting in weakness and eventual saccular outpouching of capillary walls leading to

microaneurysms, which are the earliest detectable signs of DM retinopathy that may be seen on patient

once the cataract, has been extracted.


9/18

Pathophysiology of Cataract in Diabetic Patient

Diabetic cataract is not yet fully understood, however, attributed to enzyme aldose reductase(AR) which catalyzes the reduction of glucose to sorbitol through the polyol pathway in the initiation of

the disease process. It has been shown that the intracellular accumulation of sorbitol leads to osmotic

changes resulting in hydropic lens fibers that degenerate and form sugar cataracts. In the lens of the

patient, sorbitol is produced faster than it is converted to fructose by the enzyme sorbitol

dehydrogenase. The polar character of sorbitol prevents its intracellular removal through diffusion. The

increased accumulation of sorbitol creates a hyperosmotic effect that results in an infusion of fluid to

countervail the osmotic gradient. Intracellular accumulation of polyols leads to a collapse and

liquefaction of lens fibers, which ultimately results in the formation of lens opacities that was evident of

handheld ophtalmoscope during eye examination in the ward.The Osmotic Hypothesis of sugar

cataract formation, emphasizing that the intracellular increase of fluid in response to AR-mediated

accumulation of polyols results in lens swelling associated with complex biochemical changes ultimately

leading to cataract formation. In study by Framingham published in Journal of Ophthalmology 2010

article ID 608751 cited in study by Schmidt-Erfurth in Medical University Vienna in Austria, they

mentioned 3-4x increased cataract prevalaence with DM under the age of 65 which may be applicable to

aou patient at 57 year-old and with 2x excess prevalence beyond 65 year-old and the most frequently

seen type of cataract is age-related or senile cataract which tends to occur earlier and progress more

rapidly than nondiabetic patient. They also mentioned 10 year cumulative incidence in DM type II of

24.9%.


10/18

Hypertensive Retinopathy on top of Diabetic Retinopathy

The findings of hypertensive retinopathy in this patient can also be seen only after cataract

extraction that may visualized the retina on fundoscopic examination, however, B-scan may be helpful

only when vitreous hemorrhage is present and hypertension induced changes to the retinal

microvasculature. Hypertension leads to a deposition of cholesterol into the tunica intima of medium

and large arteries. This leads to an overall reduction in the lumen size of these vessels. In

arteriolosclerosis, hypertension leads to focal closure of the retinal microvasculature that may be

aggravated by diabetic retinopathy leading to early microaneurysms. This may also gives rise to

microinfarcts (cotton wool spots) and superficial hemorrhages. It can also lead to disc edema.The

mechanism behind this phenomenon is also poorly understood like the two conditioned mentioned

above in this patient, but it may be related to a hypertension-related increase in intracranial pressure,

and hence is considered true papilledema. Again, this may only be seen once the cataract has been

extracted in patient M.A. The arteriolosclerotic changes in the retinal microvasculature persist even with

the reduction of systemic blood pressure. However, hypertensive retinopathy changes resolve over time

with the reduction of systemic blood pressure (BP). Cotton wool spots develop in 24 to 48 hours with

the elevation of BP and resolve in two to 10 weeks with the lowering of BP. A macular star develops

within several weeks of the development of elevated BP and resolves within months to years after theBP is reduced. Papilledema develops within days to weeks of increased BP and resolves within weeks to

months following BP lowering, that is why if only due to hypertension alone excluding cataract and

diabetic retinopathy the vision may be fluctuating, however, what is evident in the patient at this point

is the effects of cataract that cause gradual blurring of visual acuity of 20/400 on both eyes, negative

ROR and hazy media.

References:

Clinical Ophthalmology: A Systematic Approach by Kanski 7th

Ed.

Journal of Ophthalmology: Diabetic Cataract, Article ID 608751, Schmidt-Erfurth, et. al., 2010

Images from www.medscape.com


11/18

Parameters Diabetic Vascular Disease Case

Epidemiology Most common causes of

mortality and disability of

diabetic patients

Affects men and women,

more common in elderly

Female

54 years old

Hypertensive for 19 years

Diabetic for 24 years

Menopause at age 54

Risk factors Environmental and genetic

factors

Advanced age

Diabetes Mellitus

Dyslipidemia

Hypertension

Hypercoagulable state

54 years old

Long diabetes mellitusBP of 150/90

Poor medical compliance

Uncontrolled hypertension


History

Physical examCardiovascular

Patient has long standing

hypertension and diabetes

Left ventricular hypertrophy

Patient can feel dizziness and

light headedness

Easy Fatigability

Lateral displacement of apicalbeat into anterior midaxillary

line.

Discussion

Diabetes mellitus affects approximately 100 million persons worldwide. Five to ten percent have type 1

(formerly known as insulin-dependent) and 90% to 95% have type 2 (noninsulin-dependent) diabetes

mellitus. The incidence of type 2 diabetes arises due to lifestyle patterns contributing to obesity.In fact,

Vascular diseases are the principal causes of death and disability in people with diabetes.

Pathophysiology

In patients with diabetes, atherosclerosis is the main reason on impairment of vascular component.

Endothelial cells present on the blood vessel wall normally maintain the vascular homeostasis , ensuring

adequate blood flow and nutrient delivery while preventing thrombosis and leukocyte diapedesis.

Endothelial cells synthesized nitric oxide (NO) to promote vasodilation by activating guanylyl cyclase on

vascular smooth muscle to protect blood vessels to form endogenous injury. In addition, overproduction

of reactive oxygen species (ROS) as a result of altered glucose metabolism together with decrease on

Diabetic Vascular Diseaseby: Arlyn M. Berco


12/18

NO will permit the activity of pro inflammatory transcription factor B (NFB) leading to leukocyte

adhesion and production of cytokines and chemokines. In combination with endothelial cell insulin

resistance, these changes cause endothelial dysfunction. This will promote the monocyte and smooth

muscle migration into the intima forming macrophage foam cells. Proliferating vascular smooth muscle

cells are the major source of extracellular matrix in the atherosclerotic plaque and to the fibrous cap

covering the plaque, result in obstructed blood flow leading to diminished amounts of oxygen and

nutrients reached the target organ. Metalloproteinases released by macrophage cells will cause the

breakdown of fibrous cap and causes plaque rupture. The Exposed necrotic core and other extracellular

components to circulating blood will precipitate the major life-threatening events in atherosclerosis,

including myocardial infarction and stroke.

Complications of Vascular Diabetes

Heart disease

Damage to the heart muscle, leading to impaired relaxation and filling of the heart with blood (diastolic

dysfunction) and eventually heart failure; this condition can occurs independent of damage done to the

blood vessels over time from high levels of blood glucose.

StrokeLong standing diabetes more likely to have a stroke due to its vascular damaged done by the disease.

Plaque buildup and clot formation cause blockage in the blood vessels leading to the brain.

Peripheral arterial disease

Patients with diabetes are at risk for narrowing of the large vessels of their legs. The resulting poor

circulation impairs healing and means that even a minor injury or infection can develop into a serious

infection. A serious foot infection may travel up your leg, infect the bones, and may lead to an

amputation.
http://www.emedicinehealth.com/script/main/art.asp?articlekey=133995&ref=138000http://www.emedicinehealth.com/script/main/art.asp?articlekey=133995&ref=138000


13/18

Macrovascular complications and their symptoms

Complication Symptoms

Heart disease Chest pain or a feeling of squeezing/pressure. If you have

autonomic diabetic neuropathy, you may not have chest pain.

Decreased tolerance for physical activity

Chronicfatigue

Shortness of breath

Swelling of the legs and ankles

Palpitations

Stroke Impaired speech

Inability to see in one eye or double vision

Inability to walk

Paralysis on one side of the body

Numbness or tingling

Peripheral arterial disease

Pain in the calves when walking Coolness of the lower extremities

Loss of hair on the legs

Ulcers on the legs that do not heal promptly

Pain in the feet when resting

References

Christian Rask-Madsen, George L. King.Vascular Complications of Diabetes: Mechanisms of Injury and

Protective Factors. Cellular metabolism Volume 17, Issue 1, 8 January 2013, Pages 2033.

Healthwise Staff (Sep. 3, 2013) Macrovascular Diabetes complications.

https://myhealth.alberta.ca/health/Pages/conditions.aspx?hwid=uq1204abc 1995-2014 Healthwise,

Incorporated.
http://www.emedicinehealth.com/script/main/art.asp?articlekey=58902http://www.emedicinehealth.com/script/main/art.asp?articlekey=133955&ref=138000http://www.emedicinehealth.com/script/main/art.asp?articlekey=133955&ref=138000http://www.emedicinehealth.com/script/main/art.asp?articlekey=58902


14/18

Parameters Coronary Artery Disease Case

Epidemiology Of particular significance in

Developing Countries

African or Asian ancestry

Greatly affects men than

pre-menopausal women.

But once past the

menopause, CAD affects

both similarly.

Filipino

Female

Menopause at 54 yrs. old.

Risk Factors

Type2diabetes

Hyperlipidemia

Advanced age

High blood pressure

(hypertension)

Physical inactivity

Low socio-economic

status

Long standing DM type 2

57 yrs. old

usual blood pressure of

150/90

No routine exercise daily


History Shortness of breath

Dizziness Nausea

Feeling very tired

Orthopnea (2- pillow)

Dizziness Light headedness

Easy Fatigability

Body malaise

Physical Examination Hypertension

Poor cardiac output

Left ventricular

hypertrophy (LVH)

BP: 160/90mmHg

CRT of >2 seconds

3cm apex beat visible and

palpable at 5thICS, left

anterior axillary line

oronary rtery Diseaseby: Ve R. Orcini
http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/diabetes/http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/hypertension/http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/physical-inactivity/http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/physical-inactivity/http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/hypertension/http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/diabetes/


15/18

Discussion

CAD is the most common type of heart disease. Coronary artery disease (CAD) accounts for a large

fraction of the morbidity, mortality, and cost of diabetes.Heart diseases andstroke are the No. 1 causes

of death and disability among people with type 2 diabetes. In fact, at least 65 percent of people with

diabetes die from some form of heart disease or stroke. Adults with diabetes are two to four times more

likely to have heart disease or a stroke than adults without diabetes. The American Heart Association

considers diabetes to be one of the seven major controllable risk factors for cardiovascular disease.

Pathophysiology

In diabetes, the predominant form of LDL cholesterol is the small, dense form. Small LDL particles are

more atherogenic than large LDL particles because they can more easily penetrate and form stronger

attachments to the arterial wall, and they are more susceptible to oxidation. Coronary artery disease

occurs when part of the smooth, elastic lining inside acoronary artery (the arteries that supply blood to

the heart muscle) developsatherosclerosis.With atherosclerosis, the artery's lining becomes hardened,

stiffened, and swollen with all sorts of "gunge" - including calcium deposits, fatty deposits, and

abnormal inflammatorycells - to form aplaque.

Complications:

Coronary artery disease can lead to:

Chest pain (angina).When your coronary arteries narrow, your heart may not receive enough blood

when demand is greatest particularly during physical activity. This can cause chest pain

(angina) or shortness of breath.

Heart attack.If a cholesterol plaque ruptures and a blood clot forms, complete blockage of your heart

artery may trigger a heart attack. The lack of blood flow to your heart may damage your heart

muscle. The amount of damage depends in part on how quickly you receive treatment.

Heart failure.If some areas of your heart are chronically deprived of oxygen and nutrients because of

reduced blood flow, or if your heart has been damaged by a heart attack, your heart may

become too weak to pump enough blood to meet your body's needs. This condition is known as

heart failure.

Abnormal heart rhythm (arrhythmia). Inadequate blood supply to the heart or damage to heart

tissue can interfere with your heart's electrical impulses, causing abnormal heart rhythms.

References:Jeroen J. Bax, MD, PHD, et al. Screening for Coronary Artery Disease in Patients With Diabetes. doi: 10.2337/dc07-9927

Diabetes Care October 2007 vol. 30 no. 10 2729-2736.

Diseases and Conditions. Coronary Artery Disease. Complications.http://www.mayoclinic.org/diseases-conditions/coronary-

artery-disease/basics/complications/con-20032038. 1998-2014 Mayo Foundation for Medical Education and Research.

Lanza GA (February 2007). "Cardiac syndrome X: a critical overview and future perspectives". Heart93 (2): 15966.

doi:10.1136/hrt.2005.067330.PMC1861371.PMID16399854.

Betsy B. Dokken,PhD, NP, CDE.The Pathophysiology of Cardiovascular Disease and Diabetes: Beyond Blood Pressure and Lipids.

Diabetes Spectrum.July 2008 vol. 21 no. 3:160-165
http://www.heart.org/HEARTORG/Conditions/More/MyHeartandStrokeNews/Coronary-Artery-Disease---Coronary-Heart-Disease_UCM_436416_Article.jsphttp://www.strokeassociation.org/http://en.wikipedia.org/wiki/Coronary_arteryhttp://en.wikipedia.org/wiki/Atherosclerosishttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Atheromatous_plaquehttp://care.diabetesjournals.org/search?author1=Jeroen+J.+Bax&sortspec=date&submit=Submithttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861371http://en.wikipedia.org/wiki/Digital_object_identifierhttp://dx.doi.org/10.1136%2Fhrt.2005.067330http://en.wikipedia.org/wiki/PubMed_Centralhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861371http://en.wikipedia.org/wiki/PubMed_Identifierhttp://www.ncbi.nlm.nih.gov/pubmed/16399854http://spectrum.diabetesjournals.org/search?author1=Betsy+B.+Dokken&sortspec=date&submit=Submithttp://spectrum.diabetesjournals.org/search?author1=Betsy+B.+Dokken&sortspec=date&submit=Submithttp://www.ncbi.nlm.nih.gov/pubmed/16399854http://en.wikipedia.org/wiki/PubMed_Identifierhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861371http://en.wikipedia.org/wiki/PubMed_Centralhttp://dx.doi.org/10.1136%2Fhrt.2005.067330http://en.wikipedia.org/wiki/Digital_object_identifierhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861371http://care.diabetesjournals.org/search?author1=Jeroen+J.+Bax&sortspec=date&submit=Submithttp://en.wikipedia.org/wiki/Atheromatous_plaquehttp://en.wikipedia.org/wiki/Cell_(biology)http://en.wikipedia.org/wiki/Atherosclerosishttp://en.wikipedia.org/wiki/Coronary_arteryhttp://www.strokeassociation.org/http://www.heart.org/HEARTORG/Conditions/More/MyHeartandStrokeNews/Coronary-Artery-Disease---Coronary-Heart-Disease_UCM_436416_Article.jsp


16/18

Diabetic hyperglycemic hyperosmolar syndrome (HHS) is a complication of type 2 diabetes that involves

extremely high blood sugar(glucose) levels without the presence of ketones. Ketones are by products of

fat breakdown. It is a serious condition most frequently seen among older person. It is also usually

brought on something else, such as an illness or infection.

In HHNS, blood sugar levels rise, and your body tries to get rid of the excess sugar by passing it into your

urine. You make lots of urine at first, and you have to go to the bathroom more often. Later you may not

have to go to the bathroom as often, and your urine becomes very dark. Also, you may be very thirsty.

Even if you are not thirsty, you need to drink liquids. If you don't drink enough liquids at this point, you

can get dehydrated.

If HHNS continues, the severe dehydration will lead to seizures, coma and eventually death. HHNS may

take days or even weeks to develop.

Parameters HHS Case

Epidemiology

Causes

Age(Elderly)

DM affects men and women with equal

frequency.

Common complication of type 2

diabetes mellitus.

Extremely high blood sugar

Extreme lack of water (dehydration)

Decreased conciousness

M.A. 57y/o Female

Advanced age

The patient is diabetic

Type 2 DM

uncontrolled

Uncontrolled diabetes

Risk Factors

Concurrent illness such as myocardial

infarction or stroke Congestive heart

failure Sepsis, pneumonia, and other

serious infections, debilitating

condition. Limited access to water

Poor kidney function

Poor management of diabetes

Uncontrolled Hypertension

Uncontrolled Diabetes

Patient cannot move her

lower extremities

Patients legs and feet areweak.

Chronic Kidney Disease

Non-Compliant to her

medications

Hyperglycemic Hyperosmolar Stateby: Jimmy R. Padrinao


17/18

Physical Findings: Profound dehydration

Hyperosmolality and reveals

hypotension, tachycardia and altered

mental status. Various changes

(complete lucidity-disorientation-

lethargy-COMA)

Confusion

Convulsions

Fever

Increased thirst

Increased urination

Lethargy

Weight Loss

Weakness

Nausea Vomiting

Coma

Dysfunctional movement

Loss of feeling or function of muscles

Speech impairment

Patient had 3 episodes of

non-projectile vomiting

Patient is non- ambulatory

She is chronically ill-looking

and prefers to keep her eyes

closed.

(+) weight loss of 10% in 5

years

(+)Polyuria and Polydypsia

(+)Patients legs and feet are

weak

Discussion:

The prototypical patient with HHS is an elderly individual with type 2 DM, with a several week/years

history of polyuria, weight loss, and diminished oral intake that may culminates mental confusion,

lethargy and coma.

Normally, the kidneys try to make up for high glucose levels in the blood by allowing the extra glucose to

leave the body in the urine. If you do not drink enough fluids, or you drink fluids that contain sugar, the

kidneys can no longer get rid of extra glucose. Glucose levels in the blood can become very high as a

result. The blood then becomes much more concentrated than the normal (HYPEROSMOLARITY).

Hyperosmolarity is a condition in which the blood has a higher concentration of salt (Sodium), glucose

and other substances that normally cause water to move into the bloodstream. This draws the water

out the bodys other organs, including the brain. Hyperosmolarity creates a cycle of increasing blood

glucose levels and dehydration .

Patient M.A. elderly with long standing Diabetes mellitus, non-ambulatory, with a history of vomiting

and chronically ill-looking (prefers to keep her eyes closed) have a higher chance of developing an acute

complication of Diabetes mellitus (Hyperglycemic Hyperosmolar State HHS) .


18/18

Pathophysiology

The initiating event in hyperosmolar hyperglycemic state is glucosuric diuresis. Glucosuria impairs the

concentrating capacity of the kidney, further exacerbating water loss. Under normal conditions, the

kidney act as a safety valve to eliminate glucose above a certain threshold and prevent further

accumulation. However, decreased intravascular volume or underlying renal disease decreases the

glomerular filtration rate (GFR), causing the glucose level to increase. The loss of more water than

sodium leads to hyperosmolarity. Insulin is present, but it is not adequate to reduce blood glucose levels

particularly in the presence of significant insulin resistance.

Complication of HHS:

1.

Hyperviscosity increases risk of thrombosis

2.

Altered mental status

3.

Neurologic signs including focal signs such as sensory or motor impairments or focal seizures or

motor abnormalities, including flaccidity, depressed reflexes, tremors or fasciculations.

4.

Untreated, will lead to death.

Complications of treatment(HHS):

1.

Inadequate treatment Vascular occlusion (e.g. mesenteric artery occlusion, myocardial

infarction, low-flow syndrome and disseminated intravascular coagulopathy) and

rhabdomyolysis.

2.

Hyperviscosityincreased risk of thrombosis.

3.

OverhydrationAdult respiratory distress syndrome and induced cerebral edema.

References:

HARRISONS (Principles of INTERNAL MEDICINE 17thEDITION)

Hyperosmolar HyperglycemicNonketotic Syndrome (HHNS) Retrieved 6 July 2012

U.S. Department of Health and Human Services National Institutes of Health

Page last updated: 15 August 2014

chronic kidney disease complications

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