CEFOTAXIM 1 GR INJEKSI Komposisi : CEFOTAXIME 500 mg Tiap vial mengandung: Cefotaxime sodium setara dengan cefotaxime 500 mg CEFOTAXIME

1 g Tiap vial mengandung: Cefotaxime sodium setara dengan cefotaxime 1.000 mg Indikasi : Infeksi-infeksi yang disebabkan oleh kuman yang sensitif terhadap cafotaxime antara lain: - Infeksi saluran pemafasan bagian bawah (termasuk pneumonia). - Infeksi kulit dan struktur kulit. - Infeksi tulang dan sendi. - Infeksi intra-abdominal. - infeksi saluran kemih, - Infeksi pada alatkelaminwanita. - Meningitis. - Septikemia. - Bakteremia. - Belum terdapat data klinis yang cukup untuk mendukung pengobatan terhadap infeksi yang disebabkan oleh Salmonella typhidan infeksiparatyphi Adan B. - Tidakefektif terhadap Treponemapallidum dan Ciostridium difficile. - Pada infeksi parah dimana jiwa penderita terancam, kombinasi cefotaxime dengan aminoglikosida dapat diberikan tanpa menunggu hasil tes sensitivitas. Kedua sediaan tersebut harus diberikan secara terpisah, tidak dicampur daiam satu syringe. - infeksi karena Pseudomonas aeruginosa memerlukan pengobatan dengan antibiotika lain yang efektif terhadap Pseudomonas. Kontra indikasi : Penderita yang hipersensitif terhadap antibiotika sefalosporin. Pada penderita yang hipersensitif terhadap penisilin, kemungkinan terjadinya reaksi silang harus dipikirkan.

Dosis : - Kecuali dinyatakan lain, dosis untukorang dewasadan anakdiatas 12 tahun adalah 1 gsetiap 12 jam. - Pada infeksi sedang sampai berat: 1 -2 g setiap 6-8 jam. - Pada infeksi berat atau membahayakan diperlukan 2 g setiap4 jam. - Dosis maksimum yang dianjurkan adalah 12 g per hah. - Untuk pencegahan infeksi yang terjadi setelah operasi: 1 g IM atau IV30-90 menit sebelum pembedahan. - Pada kasus operasi caesar : 1 g IV segera setelah umbilical cord diklem, kemudian 1 g IM atau IV 6 dan 12 jam setelah dosis pertama. Methylprednisolone Sediaan : Tablet, suspensi, injeksi, salep/krim Kelompok obat : Kortikosteroid Farmakologi Metilprednisolon adalah glukokortikoid turunan prednisolon yang mempunyai efek kerja dan penggunaan yang sama seperti senyawa induknya. Metilprednisolon tidak mempunyai aktivitas retensi natrium seperti glukokortikosteroid yang lain. Indikasi Abnormalitas fungsi adrenokortikal, penyakit kolagen, keadaan alergi dan peradangan pada kulit dan saluran pernafaan tertentu, penyakit hematologik, hiperkalsemia sehubungan denga kanker. Kontraindikasi Infeksi jamur sistemik pada pasien hipersensitif. Pemberian kortikosteroid yang lama merupakan kontraindikasi pada ulkus duodenum dan peptikum, osteoporosis

berat, penderita dengan riwayat penyakit jiwa, herpes. Pasien sedang diimunisasi. Dosis Dewasa Dosis awal dari metilprednisolon dapat bermacam macam dari 4 mg 48 mg per hari, dosis tunggal atau terbagi, tergantung keadaan penyakit. Dalam sklerosis multipel: Oral 160 mg sehari selama 1 minggu, kemudian 64 mg setiap 2 hari sekali dalam 1 bulan. Anak anak Insufisiensi adrenokortikal: Oral 0,117 mg/kg BB atau 3,33 mg per m2 luas permukaan tubuh sehari dalam dosis terbagi tiga. Indikasi lain Oral 0,417 mg 1,67 mg /kg BB atau 12,5 mg 50 mg per m2 luas permukaan tubuh sehari dalam dosis terbagi 3 atau 4. Peringatan dan perhatian Tidak dianjurkan untuk wanita hamil dan menyusui, kecuali memang benar benar dibutuhkan, dan bayi yang lahir dari ibu yang ketika hamil menerima terapi kortikosteroid ini harus diperiksa. Kemungkinan adanya gejala hipoadrenalism. Pasien yang menerima terapikortikosteroid ini dianjurkan tidak divaksinasi terhadap smallpox, juga imunisasi lain terutama yang mendapat dosis tinggi, untuk mencegah kumungkinan bahaya neurologi. Tidak dianjurkan untuk bayi dan anak anak, karena penggunaan jangka panjang dapat menghambat pertumbuhan dan perkembangan anak. Jika kortikosteroid digunakan pada pasien TBC laten atau Tuberculin Reactivity perlu dilakukan pengawasan yang teliti sebagai pengaktifan kembali penyakit yang terjadi. Ada peningkatan efek kortikosteroid pada pasien dengan hipotiroid dan sirosis.

Tidak dianjurkan penggunaan pada penderita ocular herpes simplex, karena kemungkinan terjadi perforasi kornea. Pemakaian obat obat ini dapat menekan gejala gejala klinis dari suatu penyakit infeksi. Pemakaian jangka panjang dapat menurunkan daya tahan tubuh terhadap infeksi penyakit. Efek Samping Efek samping biasanya terlihat pada pemberian jangka panjang atau pemberian dalam dosis besar, misalnya gangguan elektrolit dan cairan tubuh, kelemahan otot, retensi terhadap infeksi menurun, gangguan penyembuhan luka, meningkatnya tekanan darah, katarak, gangguan pertumbuhan pada anak anak, insufisiensi adrenal, Cushings Syndrome, osteoporosis, tukak lambung. Interaksi Obat Berikan makanan untuk meminimumkan iritasi gastrointestinal. Penggunaan bersama sama antiinflamasi non-steroid atau antireumatik lain dapat mengakibatkan risiko gastrointestinal, perdarahan gastrointestinal. Penggunaan bersama sama dengan antidibetes harus dilakukan penyesuaian dosis.

Pasien yang menerima vaksinasi terhadap smallpox, juga imunisasi lain terutama yang mendapat dosis tinggi.

Arterial Blood Gases

Arterial blood gas analysis provides information on the following : 1] Oxygenation of blood through gas exchange in the lungs. 2] Carbon dioxide (CO2) elimination through respiration. 3] Acid-base balance or imbalance in extra-cellular fluid (ECF).

Normal Blood Gases

Arterial pH 7.35 - 7.45 Venous 7.32 - 7.42

Not a gas, but a measurement of acidity or alkalinity, based on the hydrogen (H+) ions present. The pH of a solution is equal to the negative log of the hydrogen ion concentration in that solution: pH = log [H+]. PaO2 80 to 100 mm Hg. 28 - 48 mm Hg

The partial pressure of oxygen that is dissolved in arterial blood. New Born Acceptable range 40-70 mm Hg. Elderly: Subtract 1 mm Hg from the minimal 80 mm Hg level for every year over 60 years of age: 80 - (age- 60) (Note: up to age 90) HCO3 22 to 26 mEq/liter (2128 mEq/L) 19 to 25 mEq/liter

The calculated value of the amount of bicarbonate in the bloodstream. Not a blood gas but the anion of carbonic acid. PaCO2 35-45 mm Hg 38-52 mm Hg

The amount of carbon dioxide dissolved in arterial blood. Measured. Partial pressure of arterial CO2. (Note: Large A= alveolor CO2). CO2 is called a volatile acid because it can combine reversibly with H2O to yield a strongly acidic H+ ion and a weak basic bicarbonate ion (HCO3 -) according to the following equation: CO2 + H2O <--- --> H + + HCO3 B.E. 2 to +2 mEq/liter Other sources: normal

reference range is between -5 to +3. The base excess indicates the amount of excess or insufficient level of bicarbonate in the system. (A negative base excess indicates a base deficit in the blood.) A negative base excess is equivalent to an acid excess. A value outside of the normal range (-2 to +2 mEq) suggests a metabolic cause for the abnormality. Calculated value. The base excess is defined as the amount of H+ ions that would be required to return the pH of the blood to 7.35 if the pCO2 were adjusted to normal. It can be estimated by the equation: Base excess = 0.93 (HCO3 - 24.4 + 14.8(pH - 7.4)) Alternatively: Base excess = 0.93HCO3 + 13.77pH - 124.58 A base excess > +3 = metabolic alkalosis a base excess < -3 = metabolic acidosis SaO2 95% to 100% 50 - 70%

The arterial oxygen saturation.

Step by Step ABG Analysis Step One Assessing pH

Look at pH and determine if it is acidotic (<7.35), normal (7.35 - 7.45), or alkalotic (> 7.45). pH is the best overall indicator in determining the acid-base status of the patient.

Step Two - Determine respiratory involvement

Review the PaCO2 to assess respiratory involvement [The lungs control the level of carbon dioxide in the arterial blood]. The PaCO2 must be evaluated in light of the arterial pH. That is, if the pH is abnormal, we then ask ourselves: would this observed PaCO2, by itself, cause this pH abnormality? For example, suppose that the pH is below 7.35 (denoting acidosis) and the PaCO2 is above 45 mmHg. According to the Henderson-Hasselbalch equation, a high PaCO2 would indeed cause a low pH (i.e., acidosis). Therefore we know that the respiratory system is at least in part, if not entirely, responsible for the acidosis. On the other hand, if the pH is less than 7.35 and the PaCO2 is in the normal range, then we know that the acidosis must be of non-respiratory (metabolic) origin. PaCO2: Normal: 35 - 45 mmHg (4.6 - 6 kPa) Respiratory acidosis: > 45 mmHg (> 6 kPa) Respiratory alkalosis: <35 mmHg (< 4.6 kPa)

Step Three - Determine metabolic involvement

Review the plasma [HCO3-] or B.E. (Base excess) to determine metabolic involvement (both controlled by non-respiratory factors.) Each of these components must be evaluated based on the current pH. If the pH is abnormal, we ask: would this observed [HCO3-] by itself, cause this pH abnormality? For example, suppose that the pH is less that 7.35 (denoting acidosis) and the [HCO3-] is below 22 mEq/L. Indeed, according to the Henderson-Hasselbalch equation, the low [HCO3-] is consistent with acidosis. Thus, we know that non-respiratory factors are in part, if not entirely, responsible for the acidosis. If [HCO3-] were in the normal range in the presence of this acidosis, then we would know that the acidosis must be of respiratory origin. HCO3-------------------------Normal: 22 - 26 mEq/L Metabolic acidosis: <22 mEq/L Metabolic alkalosis: > 26 mEq/L [Standard Bicarbonate: Calculated value. Similar to the base excess. It is defined as the calculated bicarbonate concentration of the sample corrected to a PCO2 of 5.3kPa (40mmHg). BE (Base Excess): -------------------------Normal: -2 to +2 mmol/L Metabolic acidosis: < -2 mmol/L Mild Moderate Marked Severe -4 to -6 -6 to -9 -9 to -13 to < -13

Metabolic alkalosis: > +2 mmol/L Severe Marked Moderate Mild > +13 9 to 13 6 to 9 4 to 6

[Base excess (BE) is the mmol/L of base that needs to be removed to bring the pH back to normal when PCO2 is corrected to 5.3 kPa or 40 mmHg. During the calculation any change in pH due to the PCO2 of the sample is eliminated, therefore, the base excess reflects only the metabolic component of any disturbance of acid base balance.]

Step Four - Assess for compensation

Look at the pH, PaCO2, and B.E. / HCO3- to decide whether compensatory mechanisms are at work. Once the acid-base disorder is identified as respiratory or metabolic, we must look for the degree of compensation that may or may not be occurring. we know that the system not primarily responsible for the acid-base abnormality must assume the responsibility for returning the pH to the normal range. This compensation may be complete (pH is brought into the normal range) or partial (pH is still out of the normal range but is in the process of moving toward the normal range.) In pure respiratory acidosis (high PaCO2, normal [HCO3-], and low pH) we would expect an eventual compensatory increase in plasma [HCO3-] that would work to restore the pH to normal. Similarly, we expect respiratory alkalosis to elicit an eventual compensatory decrease in plasma [HCO3-]. A pure metabolic acidosis (low [HCO3-], normal PaCO2, and a low pH) should elicit a compensatory decrease in PaCO2, and a pure metabolic alkalosis (high [HCO3-], normal PaCO2, and high pH) should cause a compensatory increase in PaCO2. All compensatory responses work to restore the pH to the normal range (7.35 - 7.45) [ See sample problems near the bottom of the page]

Step Five - Further analysis in cases of METABOLIC ACIDOSIS

Metabolic acidosis: 1] Calculate the anion gap: Anion gap = Na+ - [CL- + HCO3-] Difference between calculated serum anions and cations. Based on the principle of electrical neutrality, the serum concentration of cations (positive ions) should equal the serum concentration of anions (negative ions). However, serum Na+ ion concentration is higher than the sum of serum Cl- and HCO3- concentration. Na+ = CL- + HCO3- + unmeasured anions (gap). Normal anion gap: 12 mmol/L (10 - 14 mmol/L) 2] Based on the anion gap and patient history - review potential causes: Normal anion gap (hyperchloremic) metabolic acidosis: Normal anion gap acidosis: The most common causes of normal anion gap acidosis are GI or renal bicarbonate loss and impaired renal acid excretion. Normal anion gap metabolic acidosis is also called hyperchloremic acidosis, because instead of reabsorbing HCO3- with Na, the kidney reabsorbs Cl-. Many GI secretions are rich in bicarbonate (eg, biliary, pancreatic, and intestinal fluids); loss from diarrhea, tube drainage, or fistulas can cause acidosis. In ureterosigmoidostomy

(insertion of ureters into the sigmoid colon after obstruction or cystectomy), the colon secretes and loses bicarbonate in exchange for urinary Cl- and absorbs urinary ammonium, which dissociates into NH3+ and H+. Loss of HCO3 ions is accompanied by an increase in the serum Clconcentration. The anion gap remains normal. Disease processes that can lead to normal anion gap (hyperchloremic) acidosis. Useful mnemonic (DURHAM): a) Diarrhea (HCO3- and water is lost). b) Ureteral diversion: Urine from the ureter may be diverted to the sigmoid colon due to disease (uretero-colonic fistula) or after bladder surgery. In such an event urinary Cl- is absorbed by the colonic mucosa in exchange for HCO3-, thus increases the gastrointestinal loss of HCO3-. c) Renal tubular acidosis: dysfunctional renal tubular cells causes an inappropriate wastage of HCO3- and retention of Cl-. d) Hyperalimentation e) Acetazolamide f) Miscellaneous conditions: They include pancreatic fistula, cholestyramine, and calcium chloride (CaCl) ingestion, all of which can increase the gastrointestinal wastage of HCO3-. Increased anion gap metabolic acidosis High anion gap acidosis: The most common causes of a high anion gap metabolic acidosis are ketoacidosis, lactic acidosis, renal failure, and toxic ingestions. Renal failure causes anion gap acidosis by decreased acid excretion and decreased bicarbonate reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap. Toxins may have acidic metabolites or trigger lactic acidosis. In increased anion gap metabolic acidosis, the nonvolatile acids are organic or other inorganic acids (e.g., lactic acid, acetoacetic acid, formic acid, sulphuric acid). The anions of these acids are not Cl- ions. The presence of these acid anions, which are not measured, will cause an increase in the anion gap. Useful mnemonic (MUD PILES): Methanol poisoning: Methanol is metabolized by alcohol dehydrogenase in the liver to formic acid. Uremia: In end-stage renal failure in which glomerular filtration rate falls below 1020 ml/min, acids from protein metabolism are not excreted and accumulate in blood. Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a build up of beta-hydroxybutyric and acetoactic acids (ketoacids). Paraldehyde poisoning. Ischemia: causes lactic acidosis. Lactic acidosis: Lactic acid is the end product of glucose breakdown if pyruvic acid, the end product of anaerobic glycolysis, is not oxidized to CO2 and H2O via the

Tricarboxylic Acid Cycle. (Causes: hypoxia, ischemia, hypotension, sepsis). Ethylene glycol poisoning: Ethylene is metabolized by alcohol dehydrogenase to oxalic acid in the liver. Usually there is also a coexisting lactic acidosis. Salicylate poisoning

Causes of common acid-base disturbances: Metabolic acidosis (non-respiratory)

High anion gap. Ketoacidosis (diabetes, chronic alcoholism, malnutrition, fasting). Lactic acidosis. Renal failure. Toxins metabolized to acids: Methanol (formic acid) Ethylene glycol (oxalate) Paraldehyde (acetate, chloracetate) Salicylates Toxins causing lactic acidosis CO2 Cyanide Iron Isoniazid Toluene (initially high gap, subsequent excretion of metabolites normalizes gap) Rhabdomyolysis (rare) Loss of base Normal anion gap (hyperchloremic acidosis) GI HCO3- loss (diarrhea, ileostomy, colostomy, enteric fistulas, use of ionexchange resins) Ureterosigmoidostomy, ureteroileal conduit Renal HCO3- loss: Tubulointerstitial renal disease. Renal tubular acidosis, types 1, 2, 4. Hyperparathyroidism. Ingestions (acetazolamide, CaCl2, MgSO4) Others Hypoaldosteronism, Hyperkalemia Parenteral infusion of arginine, lysine, NH4Cl. Rapid NaCl infusion. Toluene (late). Formulas (Compensation): pCO2 decreases 1.2 for each mEq/L change in HCO3 or pCO2 = last two digits of pH Compensation Ventilation of the lungs increases through stimulation of central chemoreceptors (H+ ion receptors) in the medulla and peripheral chemoreceptors in the carotid and aortic bodies. Consequently PCO2 falls below normal, and H+ ion concentration falls. Respiratory compensation increases the acidic pH towards normal. The respiratory system responds to metabolic acidosis quickly and predictably by hyperventilation, so much so that pure metabolic

acidosis is seldom seen.

Respiratory Alkalosis:
CNS disorders or lesions, hypoxia [Hypoxia-causing conditions], pulmonary receptor stimulation (asthma, pneumonia, pulmonary edema, PE), Pulmonary vascular disease, anxiety, fear, pain, drugs (ASA, theophylline), liver failure, sepsis. Formulas (Compensation): - Acute: HCO3 decreases 0.22 for every mmHg change in pCO2 - Chronic: HCO3 decreases 0.5 for every mmHg change in pCO2

Compensation: In the presence of respiratory alkalosis the kidneys compensate for the increase in pH by retaining H+ ions and excreting HCO3 - ions. As a result, pH falls towards normal and HCO3 - concentration falls below normal. Renal compensation to respiratory alkalosis is a slow process and the pH does not completely return to normal.

Metabolic (non-resp) alkalosis:

Increase in base Administration/ingestion of HCO3Hypochloremia (HCO3 retained). Diuretic therapy Contraction of blood volume. Loss of fixed acid. Severe vomiting (loss of H+). Nasogastric suction. Hypokalemia - Potassium deficiency. Corticosteroid administration. Formulas (Compensation): pCO2 increases 0.6 for each mmol/L change in HCO3 Compensation: The respiratory response to metabolic alkalosis is hypoventilation. PCO2 rises above normal. Respiratory compensation to metabolic

Respiratory Acidosis:
Central nervous depression: sedatives etc. Neuromuscular disease (Guillain-Barr, myasthenia gravis). Trauma. Severe restrictive disorders: scoliosis. COPD. Acute airway obstruction: choking etc. CVA, pneumothorax, chest wall disorder, tumor. Acute and chronic lung disease. Formulas (Compensation): - Acute: HCO3 increases 0.1 for every mmHg change in pCO2 - Chronic: HCO3 increases 0.35 for every mmHg change in pCO2 Compensation: In the presence of respiratory acidosis the kidneys compensate for the fall in pH by excreting H+ ions

alkalosis is variable and unpredictable. It is unlikely that a conscious patient breathing spontaneously will hypoventilate to a PCO2 > 7.3 kPa (55 mmHg) to compensate for metabolic alkalosis.

and retaining HCO3 - ions. As a result, pH rises towards normal and HCO3 - concentration rises above normal. Renal compensation (also called metabolic compensation) to respiratory acidosis is a slow process. Compensation is not obvious for several hours and takes 4 days to complete.

Sample Problems - Arterial Blood Gases

Respiratory alkalosis (chronic alveolar hyperventilation) pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE: 7.44 24 16 -6 7.38 76 42 +14 7.56 44 38 +14 7.26 56 24 -4 7.56 40 34 +11 7.44 26 18 -4

Respiratory acidosis. Chronic ventilation failure

Uncompensated metabolic alkalosis

(Respiratory acidosis. acute ventilation failure

uncompensated metabolic alkalosis

Respiratory alkalosis (chronic alveolar hyperventilation)

Respiratory acidosis. Chronic ventilation failure

pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE: pH: PaCO2 : HCO3: BE:

7.40 56 34 +7 7.44 20 16 -7 7.24 36 14 -13 7.52 28 22 +1

Respiratory alkalosis. Chronic alveolar hyperventilation

Uncompensated metabolic acidosis

Respiratory alkalosis (acute alveolar hyperventilation)

Acute Respiratory Acidosis

Dx - heroin overdose. Breathing - shallow, slow. ABGs: pH: 7.30 PaCO2: 55 mm/Hg HCO3-: 27 mEq/L

Hx/Dx: 73yo, emphysema, labored breathing at rest. ABGs: Chronic Respiratory Acidosis pH: 7.36 PaCO2: 64 mmHg HCO3-: 35 mEq/L Hx/Dx: 77yo, anxiety, psychosomatic origin. Rapid breathing and slurred speech. ABGs: pH: 7.57 PaCO2: 23 mmHg HCO3-: 21 mEq/L Persistent bacterial pneumonia. Mild cyanosis and labored breathing. ABGs: pH: 7.44 PaCO2: 26 mmHg HCO3-: 17 mEq/L

Acute Respiratory Alkalosis

Compensated Respiratory Alkalosis

PaO2: 53 mmHg 80 yo with heart disease. RX: diuretic ABGs: pH: 7.58 PaCO2: 48 mmHg HCO3-: 44 mEq/L BE: + 19 mEq/L Serum CL- 95 mEq/L

Metabolic Alkalosis