Complications
Complications, complications, diabetes mellitus can be divided into two categories:(
1). Metabolik acute complications, and
(2) complications, long-term complications vaskular.
Metabolik complications due to diabetes is a relatively acute changes of plasma glucose level. Complications metabolik the most serious is ketoasidosis metabolik. Ketoasidosis metabolik is diabetes mellitus in the emergency (DM) type 1. With governance like the adekuat, mortality can be up to 2%. KAD is the definition of blood sugar> 300 mg / dl, ketonemia, and asidosis (pH <7.32 and bicarbonate level <15 mEq / L. Diagnostic step in handling ketoasidosis metabolik is:
1. Anamnesis
New cases of type 1 DM manifestation often as KAD so DM is the classic manifestation poliuria, polidipsia, and polifagia can be found. Symptoms such as respiratory asidosis complaint as quickly and in (Kussmaul) breathing aseton with the smell. Ketonemia akan seen as the body weight decreased due to the process glikoneogenesis and glikolisis. In many circumstances KAD (pH <7.1 and serum bicarbonate level <10 mEq / L) patients coming in shock treatment with or without commas. Type 1 DM patients' long, often accompanied by additional symptoms such as stomach aches and malaise. We are cautious of KAD dehydration when we find heavy going but still poliuria.
2. Physical examination
On physical examination can be found asidosis symptoms, dehydration and weight are with or without a shock, even coma.
3. Supplementary examination
Supporting the initial examination is the main blood sugar (> 300 mg / dl), urinalisis (ketonuria), and blood gas analysis (pH <7.3).> 15 mEq / L, sugar blood <200> 7.3) then the patient fasting. The calculation of fluid needs resusitasi total sedah including liquids to overcome the shock. If found hipernatremia so long resuscitate fluids given during 72 hours. Resusitasi early types of liquids used is 0.9% NaCl. When blood sugar is down to reach <250 mg / dl liquid replaced with dextrose 5% in NaCl 0.45%. The increased length of the resilience of children living with diabetes with the increasing prevalence of complications of the eye mikrosirkulasi (retinopati), kidney (nefropati), nerve (neuropati), large blood vessel (aterosklerosis), and lens (cataract). Retinopati have 45-60% of insulin dependent diabetes after 20 years and the disease is known in 20% after 10 years have clouded the lens in at least 5% of those aged less than 19 years. Nefropati diabetik also prevalent; nefropati this have on the approximately 40% of patients after 25 years suffering from insulin dependent diabetes that occurs during the starting children complications can cause death of approximately 50% of insulin dependent diabetes in the long term. Vaskular long-term complications of diabetes involves a small tube-tube (mikroangiopati) and duct-vein are large and (makroangipati). Mikroangiopati is lesi specific diabetes and that the capillary arteriola retina (retinopati diabetik), glomerolus kidney (nefropati diabetik) and nerve-nerve perifer (neuropati diabetik), musculature and skin. Be seen from the point of histokimia, thick is accompanied by the increased hoarding glikoprotein. In addition, because the chemical compound from the membrane can be derived from the basic glucose, the increased speed hiperglikemia cause the formation of cell-cell membrane basis. The use of glucose from the cells do not require insulin. There is a strong connection between hiperglikemia with insidens and development retinopati. Early manifestation retinopati form mikroaneurisma (dilation sakular small) from arteriola retina. As a result, bleeding occurred, and the network neovaskularisasi scar the retina can lead to blindness. The most successful treatment for retinopati is fotokoaguasi retina. Laser focused on the retina, resulting in scar korioretinal. After several series of rays, it will be produced about 1800 that are placed on the scar posterior polar retina. Treatment in this way appears to be pressing and bleeding that neovaskularisasi them. Early manifestation nefropati form proteinuria and hypertension. If the loss function nefron continued development, the patient will suffer insufiensi kidney and uremia. At this stage, patients may require dialysis or kidney transplant. Neuropati and cataracts occur as a result of the interference path poliol (glucose sorbitol → → fruktosa) due to lack of insulin. There is a storehouse sorbitol in the lens so that the result in the formation of cataracts and blindness. Nerve occurs in the network and fruktosa hoarding sorbitol and a decrease in the degree mioinositol cause neuropati. Changes in biochemistry network will disrupt nerve cell activity metabolik-Schwann cell and cause a loss of akson. Speed of motor conduction will be reduced at the early stage neuropati travel. Further pain relief, parestesia, reduced sensation and shakes proprioseptik, and motor disturbances that accompanied the loss of conditioned-reflex in the tendon, muscle weakness and atrofi. Neuropati can attack nerve-nerve perifer (mononeuropati and polineuropati), nerve-nerve kranial or autonomous nervous system. Attacked autonomous nervous system can nokturnal accompanied by diarrhea, stomach evacuation delay, hipotensi postural and impotensi. Makroangiopati diabetik have a picture histopatologis form aterosklerosis. Combination of disturbances caused by a biochemistry insufiensi insulin can be a cause of this type of disease vaskular. Interference-interference in the form of:
(1) hoarding sorbitol in the intima vaskular,
(2) hiperlipoproteinemia, and
(3) aberration thrombosis.
In the end makroangipati diabetik this will result in stoppage vaskular. If the arterial-arterial perifer, it can lead to insufiensi vaskular perifer with the klaudikasio intermiten and gangren in the extremity. If that is exposed koronaria and arteria aorta, it can lead to angina and infark miokardium. Third of children with diabetes experience kontraktur joints, especially in the fifth finger. But this is usually not crippling. Retinopati diabetik weight and nefropati early going in 1 / 3 of adolescent puber and young adults who had suffered from diabetes for 10-20 years. Retina changes light, such as mikroaneurisma more often found. Complications of the kidney and retina presumably more common in patients with long-term glucose control is poor or the blood pressure is higher. Gland enlargement tiroid found 20% in adolescents with diabetes and 5% have a TSH level that boast (tiroiditis subklinis). Psychological problems also seem to occur more frequently in adolescents with IDDM. Fortunately slowing growth and hepatomegali (Mauriac syndrome) because of poor glucose control is now quite rare chronicles. Also because that is based on ketoasidosis rekuren almost always caused forget inject insulin, incidence of this problem has been much reduced. Other complications described in the child's diabetes is accompanied by a shrimp heart is full of glikogen (Mauriac syndrome), osteopenia, and the syndrome of limited joint movement along with the skin tight and wax, growth interruption, and delay maturasi. Mauriac syndrome is clearly associated with lack of insulin; now rare because of the availability insulin powerless longer. Limited movement of joints syndrome is often accompanied by the development of early complications mikrovaskuler diabetik, such as retinopati and nefropati, which can appear before 18 years. None of these complications that have been diperagakan on identical twin nondiabetik, even after 20 years diabetes known depends on the twin insulin. However, as shown, predisposisi on the genetic development of diabetes complications vaskuler play an important role.
No comments:
Post a Comment