- •ICU Protocols
- •Preface
- •Acknowledgments
- •Contents
- •Contributors
- •1: Airway Management
- •Suggested Reading
- •2: Acute Respiratory Failure
- •Suggested Reading
- •Suggested Reading
- •Website
- •4: Basic Mechanical Ventilation
- •Suggested Reading
- •Suggested Reading
- •Websites
- •Suggested Reading
- •Websites
- •7: Weaning
- •Suggested Reading
- •8: Massive Hemoptysis
- •Suggested Reading
- •9: Pulmonary Thromboembolism
- •Suggested Reading
- •Suggested Reading
- •Websites
- •11: Ventilator-Associated Pneumonia
- •Suggested Readings
- •12: Pleural Diseases
- •Suggested Reading
- •Websites
- •13: Sleep-Disordered Breathing
- •Suggested Reading
- •Websites
- •14: Oxygen Therapy
- •Suggested Reading
- •15: Pulse Oximetry and Capnography
- •Conclusion
- •Suggested Reading
- •Websites
- •16: Hemodynamic Monitoring
- •Suggested Reading
- •Websites
- •17: Echocardiography
- •Suggested Readings
- •Websites
- •Suggested Reading
- •Websites
- •19: Cardiorespiratory Arrest
- •Suggested Reading
- •Websites
- •20: Cardiogenic Shock
- •Suggested Reading
- •21: Acute Heart Failure
- •Suggested Reading
- •22: Cardiac Arrhythmias
- •Suggested Reading
- •Website
- •23: Acute Coronary Syndromes
- •Suggested Reading
- •Website
- •Suggested Reading
- •25: Aortic Dissection
- •Suggested Reading
- •26: Cerebrovascular Accident
- •Suggested Reading
- •Websites
- •27: Subarachnoid Hemorrhage
- •Suggested Reading
- •Websites
- •28: Status Epilepticus
- •Suggested Reading
- •29: Acute Flaccid Paralysis
- •Suggested Readings
- •30: Coma
- •Suggested Reading
- •Suggested Reading
- •Websites
- •32: Acute Febrile Encephalopathy
- •Suggested Reading
- •33: Sedation and Analgesia
- •Suggested Reading
- •Websites
- •34: Brain Death
- •Suggested Reading
- •Websites
- •35: Upper Gastrointestinal Bleeding
- •Suggested Reading
- •36: Lower Gastrointestinal Bleeding
- •Suggested Reading
- •37: Acute Diarrhea
- •Suggested Reading
- •38: Acute Abdominal Distension
- •Suggested Reading
- •39: Intra-abdominal Hypertension
- •Suggested Reading
- •Website
- •40: Acute Pancreatitis
- •Suggested Reading
- •Website
- •41: Acute Liver Failure
- •Suggested Reading
- •Suggested Reading
- •Websites
- •43: Nutrition Support
- •Suggested Reading
- •44: Acute Renal Failure
- •Suggested Reading
- •Websites
- •45: Renal Replacement Therapy
- •Suggested Reading
- •Website
- •46: Managing a Patient on Dialysis
- •Suggested Reading
- •Websites
- •47: Drug Dosing
- •Suggested Reading
- •Websites
- •48: General Measures of Infection Control
- •Suggested Reading
- •Websites
- •49: Antibiotic Stewardship
- •Suggested Reading
- •Website
- •50: Septic Shock
- •Suggested Reading
- •51: Severe Tropical Infections
- •Suggested Reading
- •Websites
- •52: New-Onset Fever
- •Suggested Reading
- •Websites
- •53: Fungal Infections
- •Suggested Reading
- •Suggested Reading
- •Website
- •55: Hyponatremia
- •Suggested Reading
- •56: Hypernatremia
- •Suggested Reading
- •57: Hypokalemia and Hyperkalemia
- •57.1 Hyperkalemia
- •Suggested Reading
- •Website
- •58: Arterial Blood Gases
- •Suggested Reading
- •Websites
- •59: Diabetic Emergencies
- •59.1 Hyperglycemic Emergencies
- •59.2 Hypoglycemia
- •Suggested Reading
- •60: Glycemic Control in the ICU
- •Suggested Reading
- •61: Transfusion Practices and Complications
- •Suggested Reading
- •Websites
- •Suggested Reading
- •Website
- •63: Onco-emergencies
- •63.1 Hypercalcemia
- •63.2 ECG Changes in Hypercalcemia
- •63.3 Superior Vena Cava Syndrome
- •63.4 Malignant Spinal Cord Compression
- •Suggested Reading
- •64: General Management of Trauma
- •Suggested Reading
- •65: Severe Head and Spinal Cord Injury
- •Suggested Reading
- •Websites
- •66: Torso Trauma
- •Suggested Reading
- •Websites
- •67: Burn Management
- •Suggested Reading
- •68: General Poisoning Management
- •Suggested Reading
- •69: Syndromic Approach to Poisoning
- •Suggested Reading
- •Websites
- •70: Drug Abuse
- •Suggested Reading
- •71: Snakebite
- •Suggested Reading
- •72: Heat Stroke and Hypothermia
- •72.1 Heat Stroke
- •72.2 Hypothermia
- •Suggested Reading
- •73: Jaundice in Pregnancy
- •Suggested Reading
- •Suggested Reading
- •75: Severe Preeclampsia
- •Suggested Reading
- •76: General Issues in Perioperative Care
- •Suggested Reading
- •Web Site
- •77.1 Cardiac Surgery
- •77.2 Thoracic Surgery
- •77.3 Neurosurgery
- •Suggested Reading
- •78: Initial Assessment and Resuscitation
- •Suggested Reading
- •79: Comprehensive ICU Care
- •Suggested Reading
- •Website
- •80: Quality Control
- •Suggested Reading
- •Websites
- •81: Ethical Principles in End-of-Life Care
- •Suggested Reading
- •82: ICU Organization and Training
- •Suggested Reading
- •Website
- •83: Transportation of Critically Ill Patients
- •83.1 Intrahospital Transport
- •83.2 Interhospital Transport
- •Suggested Reading
- •84: Scoring Systems
- •Suggested Reading
- •Websites
- •85: Mechanical Ventilation
- •Suggested Reading
- •86: Acute Severe Asthma
- •Suggested Reading
- •87: Status Epilepticus
- •Suggested Reading
- •88: Severe Sepsis and Septic Shock
- •Suggested Reading
- •89: Acute Intracranial Hypertension
- •Suggested Reading
- •90: Multiorgan Failure
- •90.1 Concurrent Management of Hepatic Dysfunction
- •Suggested Readings
- •91: Central Line Placement
- •Suggested Reading
- •92: Arterial Catheterization
- •Suggested Reading
- •93: Pulmonary Artery Catheterization
- •Suggested Reading
- •Website
- •Suggested Reading
- •95: Temporary Pacemaker Insertion
- •Suggested Reading
- •96: Percutaneous Tracheostomy
- •Suggested Reading
- •97: Thoracentesis
- •Suggested Reading
- •98: Chest Tube Placement
- •Suggested Reading
- •99: Pericardiocentesis
- •Suggested Reading
- •100: Lumbar Puncture
- •Suggested Reading
- •Website
- •101: Intra-aortic Balloon Pump
- •Suggested Reading
- •Appendices
- •Appendix A
- •Appendix B
- •Common ICU Formulae
- •Appendix C
- •Appendix D: Syllabus for ICU Training
- •Index
332 |
Shalimar and S.K. Acharya |
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Acute liver failure |
Resuscitation: A, B, C Admit to ICU. |
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Rule out other causes of fever with |
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encephalopathy |
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Clinical evaluation and assessment of |
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grade of encephalopathy, cerebral edema |
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and prognostic indicators |
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Investigate CBC, electrolytes, BUN, creatinine, RBS |
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serum bilirubin, transaminases, PT, CXR, arterial blood |
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gases, arterial ammonia daily, blood culture endotracheal |
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aspirate in intubated patients, and urine culture |
Liver transplant available: Early referral—if prognostic models support high mortality at admission
Liver transplant not available/contraindicated: Continue supportive measures
Maintenance of blood sugar, electrolytes, oxygen saturation temperature Cerebral edema: head end elevation, mannitol, intubation in grades 3–4 Prophylactic antibiotics: Third-generation cephalosporins, vancomycin, and fluconazole NAC
Improvement: Continue
No improvement: Control sepsis
supportive therapy
(antibiotics as per culture reports), supportive care
Fig. 41.1 A summary of approach to FHF
Suggested Reading
1.Bhatia V, Singhal A, Panda SK, Acharya SK. A 20-year single-center experience with acute liver failure during pregnancy: is the prognosis really worse? Hepatology. 2008;48:1577–85.
The mortality of pregnant patients with ALF is similar to that of nonpregnant women and is independent of the cause or trimester. Pregnancy per se should not be regarded as a poor prognostic factor for a patient with ALF
41 Acute Liver Failure |
333 |
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2.Acharya SK, Dasarathy S, Kumer TL, Sushma S, Prasanna KS, Tandon A, et al. Fulminant hepatitis in a tropical population: clinical course, cause and early predictors of outcome. Hepatology. 1996;23:1448–55.
The study was conducted prospectively, at a single tertiary care center in India, to document the demographic and clinical characteristics, natural course, and causative profile of patients with FHF as well as to define simple prognostic markers in these patients. The prognostic model developed in the current study is simple and can be performed at admission.
3.Riegler JL, Lake JR. Fulminant hepatic failure. Med Clin North Am. 1993;77:1057–83.
A comprehensive review of the management of fulminant hepatic failure
4.Trey C, Davidson CS. The management of fulminant hepatic failure. In: Popper H, Schaffner F, editors. Progress in liver failure. New York: Grune and Stratton; 1970. pp. 282–98.
Acute Decompensation in Chronic Liver |
42 |
Failure |
Deepak Amarapurkar
A 54-year-old male patient, diagnosed to have cryptogenic cirrhosis 3 years back, was brought to the hospital, with abnormal behavior, inability to walk, edema over the feet, and distention of the abdomen for 3 days. On examination, the patient was found conscious but disoriented, having flapping tremors, icteric with edematous feet, and moderate ascites.
Hepatic encephalopathy of any form is seen in 50–70% patients of cirrhosis. Mortality in patients of cirrhosis with encephalopathy ranges from 30% to 50% at the end of 1 year and 70% at the end of 3 years.
Step 1: Initiate resuscitation
•All patients who have altered sensorium and cannot maintain their airway require immediate attention to airway. This assessment is done mainly by clinical means.
•They should be put on high-flow oxygen to increase SpO2 to above 90%. Patients who are unable to maintain their oxygenation are put on assisted ventilation.
•Circulation needs to be maintained by fluid infusion. If clinically there is evidence of cardiac impairment, fluids should be given cautiously.
Step 2: Take history to identify precipitating factors
In a patient of cirrhosis with acute worsening, take history to identify the precipitating factors. Usual precipitating factors in acute encephalopathy are shown in Table 42.1.
D. Amarapurkar, D.M, D.N.B. (*)
Department of Gastroenterology, Bombay Hospital & Medical Research Centre, Mumbai, India
e-mail: amarapurkar@gmail.com
R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach, |
335 |
DOI 10.1007/978-81-322-0535-7_42, © Springer India 2012 |
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336 |
D. Amarapurkar |
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Table 42.1 Precipitating |
Gastrointestinal bleeding |
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factors in portosystemic |
Constipation |
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encephalopathy |
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Large protein meal |
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Psychoactive drugs |
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Electrolyte imbalance—hypokalemia and hyponatremia |
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Infections |
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Superimposed acute hepatic injury |
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Alkalosis |
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Sedation |
Step 3: Send investigations
The following investigations should be sent:
•Complete blood count
•Liver function tests including prothrombin time
•Blood glucose, urea, serum creatinine, serum electrolytes
•Blood culture
•Arterial ammonia level
•Urine examination including culture
•Chest X-ray posteroanterior view
•Ultrasound examination of the whole abdomen including liver, spleen, portal vein, kidneys, ureter, and bladder (KUB) and ascites
•Ascitic fluid examination including culture of the fluid, inoculated in the blood culture bottle at bedside
Step 4: Stage encephalopathy
Once hepatic encephalopathy is diagnosed, it should be staged as shown in Table 42.2.
Table 42.2 Clinical stages of hepatic encephalopathy
Stage |
Mental status |
Neuromuscular function |
1 |
Impaired attention, irritability, depression |
Tremor, incoordination, apraxia |
2 |
Drowsiness, behavioral changes, memory |
Asterixis, slowed or slurred speech, ataxia |
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impairment, sleep disturbances |
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3 |
Confusion, disorientation, somnolence, |
Hypoactive reflexes, nystagmus, clonus, |
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amnesia |
muscular rigidity |
4 |
Stupor and coma |
Dilated pupils and decerebrate posturing, |
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oculocephalic reflex |
Step 5: Manage hepatic encephalopathy
(A)Standard Therapeutic Measure in Hepatic Encephalopathy
•Nutritional management:
–Normal protein diet for episodic hepatic encephalopathy
–1–2 g of protein per kg/day
–Zinc replacement
42 Acute Decompensation in Chronic Liver Failure |
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•Reduction in nitrogenous load arising from the gut.
•Bowel cleansing.
•Nonabsorbable disaccharides—lactulose is a first-line pharmacological treatment for hepatic encephalopathy. Lactulose should be given to have two to three loose stools per day.
•Antibiotics—a therapeutic alternative to nonabsorbable disaccharides for treatment in acute and chronic encephalopathy and cirrhosis. Rifaximin is equally effective as lactulose. Rifaximin is used up to 1,200 mg/day in divided doses.
•Ornithine aspartate in oral or intravenous form is only useful for a short duration. It should be avoided in renal dysfunction.
•Drugs that affect the neurotransmission—flumazenil and bromocriptine administration may have a therapeutic role in selected patients.
•Manipulation of the splanchnic circulation—closure of large portosystemic shunts.
(B)Renal Failure in Cirrhosis
Step 1: Assess the renal function
•Measuring renal function in cirrhosis:
–Creatinine of more than 1.5 mg/dL is considered renal failure.
•Fallacies of measuring creatinine:
–Underestimation of severity of renal dysfunction due to poor muscle mass. Creatinine may be falsely low.
–Small changes in creatinine (0.4–0.8) may signal significant declines in glomerular filtration rate.
Step 2: Assess the cause of renal dysfunction
• Important causes of renal failure are given in Table 42.3.
Table 42.3 Causes of renal dysfunction in cirrhosis
Acute |
Chronic |
Hypovolemia |
Glomerulonephritis |
Diuretics |
Hepatitis B |
Gastrointestinal bleed |
Hepatitis C |
Diarrhea (lactulose-induced) |
IgA nephropathy (alcoholic) |
Nephrotoxic drugs |
Diabetic nephropathy |
Aminoglycosides |
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Nonsteroidal anti-inflammatory drugs |
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Contrast agents |
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Sepsis |
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Acute kidney injury |
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Step 3: Workup of renal dysfunction in patients with cirrhosis
•Evaluate to find the cause and severity of renal dysfunction in cirrhosis.
•One of the very important investigations of such a patient is urine examination (Table 42.4).
338 |
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D. Amarapurkar |
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Table 42.4 Typical urinalysis in renal dysfunction in cirrhosis |
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Osmolality |
Urine sodium |
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Protein |
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Cause |
(mOsm/kg) |
(mmol/L) |
Sediment |
(mg/day) |
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Prerenal hypovolemia |
500 |
<20 |
Normal |
<500 |
||
Hepatorenal syndrome (HRS) |
500 |
<20 |
Nil |
<500 |
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Intrinsic |
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ATN |
<350 |
> 40 |
Granular casts |
<500 |
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Acute interstitial nephritis |
<350 |
> 40 |
RBC and |
500–2,000 |
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(AIN) |
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eosinophils |
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Acute glomerulonephritis (AG) |
Variable |
Variable |
WBCs, red cell |
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casts |
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Renal failure in patients of acute |
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decompensation in chronic liver disease |
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ECF fluid losses; rapid or excessive diuresis, vomiting, diarrhea, hemorrhage, recent LVP or hemodynamic changes due to use of NSAIDs or other drugs
No
Recent use of nephrotoxic medications (aminoglycosides, radiocontrast), hypotension (sepsis, hemorrhage)
No
Glomerular proteinuria and hematuria, i.e. dysmorphic RBC,s RBC casts
No
Imaging (ultrasound, CT scan) shows hydronephrosis or urinary retention
No
Yes
Yes
Yes
Yes
Hold diuretics or other offending medications, trial of intravascular volume expander (albumin); if renal function improves, diagnosis of prerenal state is made
Toxic or ischemic ATN
Suspect glomerular disease. Depending on clinical scenario, further workup may include cryoglobulins, C3, C4, and renal biopsy
Suggestive of obstructive uropathy. Unless long standing relief of obstruction should lead to improvement in renal function
Patient has evidence of portal hypertension |
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Yes |
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Hepatorenal Syndrome |
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(ascites). Cr > 1.5 |
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Fig. 42.1 Evaluation and management of renal failure
Step 4: Diagnose and manage renal failure
•Management depends on the type of injury. If there is an obvious precipitating factor like volume depletion, it should be corrected. Nephrotoxic drugs should be stopped, and diuretics should be withheld. If there is sepsis, appropriate antibiotics should be used (Fig. 42.1).
42 Acute Decompensation in Chronic Liver Failure |
339 |
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Step 5: Identify Hepatorenal syndrome
•(HRS) HRS is a reversible functional renal impairment that occurs in patients with advanced liver cirrhosis or those with fulminant hepatic failure. It requires quick recognition of type of hepatorenal syndrome (Table 42.5) and aggressive management; otherwise outcomes are bad.
Table 42.5 Hepatorenal syndrome |
|
Type 1 |
Type 2 |
Rapid reduction in renal function in less |
Renal function slowly deteriorates over weeks |
than 2 weeks |
to months |
Doubling of initial serum creatinine |
Increase in serum creatinine to more than |
to >2.5 mg/dL or 50% Reduction of the initial |
1.5 mg/dl or creatinine clearance less |
24-h creatinine clearance to <20 mL/min |
than 40 ml/mt |
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Occurs in cirrhotic patients with refractory |
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ascites |
Severely ill patients |
Mild jaundice |
Jaundice |
Some degrees of coagulopathy |
Coagulopathy |
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Step 6: Treat hepatorenal syndrome
•Measure creatinine clearance in the patient with tense ascites.
•Use diuretics judiciously if creatinine clearance is low.
•Avoid nonsteroidal anti-inflammatory drugs.
•Avoid aminoglycosides.
•Treat volume depletion aggressively.
•Treat infection and sepsis aggressively.
•Restrict Na+ intake to 1 g/day.
• If serum Na+ is less than 125 mEq/L, restrict fluid intake.
•Treat gastrointestinal bleeding.
•Use intravenous plasma expanders and vasoconstrictors.
•Consider liver transplant if the patient has refractory ascites or refractory hypotension.
•Recommendations for the use of vasoconstrictors in patients with type 2 hepatorenal syndrome:
–The goal of treatment is to reduce serum creatinine concentrations to £1.5 mg/ dL (130 mmol/L).
–Terlipressin at a dose of 0.5 mg should be given intravenously every 4 h; the dose can be increased in a stepwise fashion (i.e., every 2 days) to 1 mg every 4 h and then up to 2 mg every 4 h in cases of where there is no reduction in the serum creatinine concentration.
–Alternatively a continuous infusion of terlipressin at a dose of 2 mg/day can be given. When the serum creatinine concentration does not reduce by at least 30%, the dose can be increased every 2 days up to 12 mg/day.