Diet

Many diet books advise people to chew slowly so they will feel full after eating less food than if they ate quickly. As we explain in the current issue  eating slowly doesn’t always work, but when it does, the reason has as much to do with the brain as with the gut.
Scientists have known for some time that a full stomach is only part of what causes someone to feel satisfied after a meal; the brain must also receive a series of signals from digestive hormones secreted by the gastrointestinal tract.
Stretch receptors in the stomach are activated as it fills with food or water; these signal the brain directly through the vagus nerve that connects gut and brainstem. Hormonal signals are released as partially digested food enters the small intestine. One example is cholecystokinin (CCK), released by the intestines in response to food consumed during a meal. Another hormone, leptin, produced by fat cells, is an adiposity signal that communicates with the brain about long-range needs and satiety, based on the body’s energy stores. Research suggests that leptin amplifies the CCK signals, to enhance the feeling of fullness. Other research suggests that leptin also interacts with the neurotransmitter dopamine in the brain to produce a feeling of pleasure after eating. The theory is that, by eating too quickly, people may not give this intricate hormonal cross-talk system enough time to work.
Of course, as anyone who has tried eating slowly in order to lose weight can attest, it’s not quite that simple. People who are obese, for example, may suffer from leptin resistance, meaning that they are less responsive to satiety or pleasure signals from this hormone. People are also sensitive to cues in the environment , such as the alluring smell of chocolate chip cookies or the sight of a juicy burger , that can trigger the desire to eat.
Appetite is complex and dieting is a challenge. Even so, people who are trying to lose weight may want to start by chewing more slowly. In that way, they allow themselves enough time to experience pleasure and satiety.
What are your thoughts about this theory? Has chewing slowly enabled you to feel full faster?

Enjoy life

One of the things I like most about Thanksgiving is the laughter around the dinner table. The food is great, make no mistake. But it’s the sounds of happiness—the high peal, the good-natured guffaw, the snort-and-shaking-shoulders, and the deep belly laugh—that really make me give thanks. Laughter isn’t just a way to stay connected with family and friends. If new research pans out, it is also doing our hearts some good.

From brain scans and other tests, neuroscientists are compiling evidence that laughter triggers chemical responses in the brain that lead to feelings of pleasure and a sense of well-being. Laughter also appears to go beyond the belly and the brain—arteries respond to it in healthy ways that could improve blood flow and long-term health. (I’m talking about “mirthful” laughter here, the kind sparked by a funny story or a Billy Crystal routine. Sarcastic or other kinds of unfriendly or hostile laughter are a different story.)

At the University of Texas, Austin, researchers asked 17 healthy adults to watch a humorous 30-minute video of their choosing or a documentary, with before and after tests of blood flow. The biggest differences between the two groups were in measures of artery function (a test called flow-mediated dilation) and flexibility (the carotid artery augmentation index). These improved immediately in the volunteers who watched a comedy and stayed that way for almost 24 hours. In those who watched a documentary, though, artery function decreased a bit.

This study builds on work done by cardiologist Michael Miller and his colleagues at the University of Maryland Medical Center. They have demonstrated similar improvements in artery function after laughing at a comedy.Why this happens is all speculation. Miller and William Fry, a psychiatrist at Stanford University School of Medicine who began studying the effects of laughter on the cardiovascular system in the 1970s, hypothesize that brain chemicals called endorphins,which are released during mirthful laughter, latch onto opiate receptors in the lining of blood vessels. This interaction stimulates blood vessels to release nitric oxide, a molecule known to relax arteries. Relaxed arteries are more flexible and wider, permitting easier blood flow.

It’s a long way from laboratory measures of improved artery function to better health and longer life. That’s why you can’t rely on laughter as your only medicine. And a laughter prescription might not be as much fun as it sounds. Instead, enjoy laughter when it comes and bless it as another thread in the web of connections  that help keep us happy and healthy.

Φυσιολογία του πόνου

συγγραφέας Δαλαμάγκα Μαρία

Τι είναι πόνος ;

Προσδίδουμε διαφορετικούς χαρακτήρες στο πόνο. Αν ένα παιδί τραυματιστεί , θα κλάψει και θα πει «έχω πληγή».Η μητέρα θα ρωτήσει: που πονάει αγάπη μου; Σκεφτείτε ότι πρόκειται για δυο διαφορετικές προσεγγίσεις στο πόνο : 1.Το συναισθηματικό στοιχείο του πόνου , που είναι φυλογενετικά πρωτόγονο και ασχολείται με το πόνο σαν κάτι δυσάρεστο , που πρέπει να αποφεύγεται και το τελευταίο πιο πρόσφατο : 2.το διακριταίο στοιχείο του πόνου , που είναι η ικανότητα να αντιλαμβάνεται ακριβώς που είναι ο πόνος και να ανταποκρίνεται κατάλληλα.

Πόνος στο φλοιό

Συνηθιζόταν να λέγεται ότι οι δομές του φλοιού μόνο επιφανειακά ασχολούνται με την αντίληψη του πόνου, αν όχι και καθόλου. Αυτό είναι λάθος , καθώς ένα πλήθος συνδέσεων , συνδέουν υψηλότερες δομές του φλοιού με κέντρα του πόνου στο θάλαμο και το εγκεφαλικό στέλεχος. Σημαντικές δομές  του φλοιού είναι :

Ο πρωτεύων αισθητικός φλοιός (sensory cortex )

O δευτερεύων αισθητικός φλοιός

Το πρόσθιο τμήμα του κεντρικού λοβού των εγκεφαλικών ημισφαιρίων ( insula )

Η προσαγωγός έλικα

Ο πρωτεύων αισθητικός φλοιός είναι υπεύθυνος για τον εντοπισμό του πόνου . Η προσαγωγός έλικα σχετίζεται με το συναισθηματικό στοιχείο του πόνου.

Ο θάλαμος

Ο θάλαμος είναι ο κεντρικός σταθμός μετάδοσης του πόνου. Αρκετοί από τους πυρήνες του ασχολούνται με το πόνο. Οι  πλάγιοι πυρήνες ασχολούνται με το αισθητικό / διακριταίο στοιχείο του πόνου και οι έσω πυρήνες με το συναισθηματικό στοιχείο του πόνου.

Μεσεγκέφαλος

Υπάρχει ένα πλήθος δομών που σχετίζονται με το πόνο στο μεσεγκέφαλο .Το μεγαλύτερο μέρος αυτού του κυκλώματος σχετίζεται με το συναισθηματικό στοιχείο του πόνου , με εκτεταμένες συνδέσεις  με το δικτυωτό σχηματισμό του εγκεφαλικού στελέχους. Σημαντικά στοιχεία είναι τα εξής :

Η περιϋδραγώγειος  φαιά ουσία

Ο ερυθρός πυρήνας

Ο πυρήνας του Darkschewitsch

Ο διάμεσος πυρήνας του Cajal

Ο σφηνοειδής πυρήνας και ο πυρήνας του Edinger – Westphal

To εγκεφαλικό στέλεχος

Το πιο σημαντικό κέντρο του πόνου στη γέφυρα είναι ο locus coeruleus (υπομέλανας τόπος) .Αυτός περιέχει νοραδρεναλίνη και νευρώνες που ρυθμίζουν το πόνο μέσω οδών, που κατέρχονται προς το νωτιαίο μυελό.

Ο προμήκης μυελός

Συμμετέχει επίσης στο συναισθηματικό στοιχείο του πόνου. Σημαντικός είναι ο γιγαντοκυτταρικός πυρήνας και ο πλάγιος δικτυωτός πυρήνας.

Ο νωτιαίος μυελός

Παραδοσιακά υπήρχε η άποψη ότι οι περισσότερες ίνες του πόνου (Αδ και C ) εισέρχονται στη φαιά ουσία των οπισθίων κεράτων του νωτιαίου μυελού. Στη συνέχεια συνάπτονται διαμέσου της ανιούσας οδού με τη νωτιαίοθαλαμική οδό. Στη πραγματικότητα , οτιδήποτε πάνω από το 40% των αισθητικών ινών εισέρχεται στη κοιλιακή ρίζα.

Υπήρξε μεγάλος ενθουσιασμός όταν περιγράφηκε για πρώτη φορά η θεωρία της πύλης (gate control ) .Αν και ο μηχανισμός έχει πλέον τεκμηριωθεί και έχει κλινική xρήση , είναι γνωστό ότι αποτελεί μια απλοποίηση. Η βασική ιδέα είναι ότι το εισερχόμενο ερέθισμα του πόνου μπορεί να διακοπεί από άλλα ερεθίσματα , διότι πολλά νευρικά κύτταρα επικοινωνούν μεταξύ τους στο οπίσθιο κέρας. Οι πιο σημαντικές ίνες οι οποίες εισέρχονται από τη περιφέρεια στο ραχιαίο κέρας είναι :

Αμύελες C ίνες που είναι σημαντικοί μεταφορείς του μεγάλης διάρκειας πόνου , που προκαλεί το χειρουργικό τραύμα.

Λεπτές εμμύελες Αδ  ίνες που σχετίζονται με έναν πιο εντοπισμένο πόνο.

Αβ ίνες  που φέρουν πληροφορίες σχετικά με την αντίληψη της θέσης από τη περιφέρεια προς το νωτιαίο μυελό

Δυσάρεστα ερεθίσματα που εισέρχονται δια των C  ινών μπορούν να κατασταλούν με ταυτόχρονη διέγερση των Α-δ ινών (ερέθισμα υψηλής έντασης και χαμηλής συχνότητας , όπως για παράδειγμα με βελονισμό ) ή από ερεθίσματα που διέρχονται από τις Α-β ίνες. Για παράδειγμα TENS : διαδερμική ηλεκτρική νευρική διέγερση και η απλή τριβή του δέρματος , η οποία είναι πολύ καλά γνωστή από τις μητέρες , ότι ελαττώνει την αντίληψη του πόνου.

Ανιούσα οδός

Νωτιαίο-δίκτυο- διεγκεφαλική οδός: έχει λίγους έως καθόλου υποδοχείς οπιοειδών . Έχει ελάχιστη σχέση με την αντίληψη του πόνου , ως  οδυνηρό ερέθισμα.

Κατιούσα οδός

Εξίσου σημαντικές είναι οι ίνες,  που κατέρχονται από το εγκεφαλικό στέλεχος στο νωτιαίο μυελό για να τροποποιήσουν τα εισερχόμενα ερεθίσματα. Νευροδιαβιβαστές είναι η νοραδρεναλίνη ειδικά στο υπομέλανα τόπο (locus  coeruleus) και η σεροτονίνη στο raphe nuclei.Οι υποδοχείς των οπιοειδών είναι ιδιαίτερα εμφανής εδώ.

Πόνος στη περιφέρεια

Οι περισσότεροι ιστοί περιέχουν ειδικούς  υποδοχείς του πόνου , οι οποίοι ονομάζονται αλγοϋποδοχείς (nociceptor ).Στο παρελθόν πίστευαν ότι το επώδυνο ερέθισμα γινόταν αντιληπτό μέσω υπερδιέγερσης των υποδοχέων. Αυτό είναι λάθος. Η ποιότητα του πόνου φαίνεται να εξαρτάται από τη περιοχή διέγερσης και τη φύση των ινών που διαβιβάζουν την αίσθηση του πόνου. Ακόμη και στη περιφέρεια , υπάρχει μια διάκριση ανάμεσα στο οξύ άμεσο πόνο («ο πρώτος πόνος») διαβιβαζόμενος από τις Αδ ίνες και ο παρατεταμένος δυσάρεστος καυστικός πόνος , που διαβιβάζεται από μικρότερες αμύελες C ίνες.

Οι αλγοϋποδοχείς έχουν πολλούς διαφορετικούς υποδοχείς στην επιφάνεια τους , που διαμορφώνουν την ευαισθησία τους στη διέγερση. Αυτοί περιλαμβάνουν τους  GABA , τη βραδυκινίνη , την ισταμίνη , τη σεροτονίνη , τους υποδοχείς της καψαϊκίνης , τα οπιούχα , αλλά οι ποικίλοι ρόλοι αυτών των υποδοχέων ελάχιστα αναφέρονται.

Το πιο εντυπωσιακό , όσον αφορά την αντίληψη του πόνου στη περιφέρεια , είναι ότι οι περισσότεροι αλγοϋποδοχείς παραμένουν αδρανείς. Η φλεγμονή ευαισθητοποιεί τη μεγαλύτερη πλειοψηφία των αλγοϋποδοχέων και τους οδηγεί σε μια μεγαλύτερη ευαισθησία στη διέγερση (υπεραλγησία ).Η υπεραλγησία μπορεί να είναι πρωτογενής (αισθητή στη περιοχή της διέγερσης , σχετιζόμενη με την ευαισθητοποίηση των νευρώνων αυτού του δερμοτομίου ) ή δευτερογενής (αισθητή σε μια απομακρυσμένη περιοχή απ΄το πρωταρχικό τραύμα και πιθανώς σχετίζεται με τη διαμεσολάβηση των NMDA  « wind up».

Νευροδιαβιβαστές

Ένα πλήθος νευροδιαβιβαστών διαμεσολαβούν τη μεταβίβαση της αίσθησης του πόνου , τόσο στον εγκέφαλο , όσο και στο νωτιαίο μυελό. Ο αριθμός των νευροδιαβιβαστών αυξάνεται καθημερινά. Μπορούμε να τους ταξινομήσουμε στις εξής κατηγορίες :

Διεγερτικοί: glutamate (γλουταμικό )και ταχυκινίνες

Ανασταλτικοί: Υπάρχουν πολλοί ανασταλτικοί νευροδιαβιβαστές , αλλά στο ΚΝΣ , το GABA ( γ-αμινοβουτυρικό οξύ ) φαίνεται να κυριαρχεί.

Οι νευροδιαβιβαστές που εμπλέκονται στη φυγόκεντρη ρύθμιση του πόνου. Οι άλφα- 2  διεγερτικές επιδράσεις της νοραδρεναλίνης και οι δράσεις της σεροτονίνης είναι εμφανής. Τα οπιοειδή ανακουφίζουν από το πόνο , ενεργοποιώντας τους μ- και δ- υποδοχείς.  

STROKE

Stroke has always been a much-feared medical emergency, and rightly so. Someone in the United States has a stroke every 40 seconds, and someone dies of a stroke every four minutes, amounting to 795,000 strokes and 137,000 deaths annually. Stroke is the third leading cause of death in the United States, behind heart disease and cancer.

Not all strokes are preventable, so it is very important to recognize the early signs of stroke and get treatment as rapidly as possible. Stroke damages brain tissue, but that loss can be minimized by getting quickly to an emergency room that can connect to a rapid-response stroke center.

Everyone should learn the following warning signs of stroke. If you experience any of these symptoms, immediately dial 911 or go to an emergency room:

weakness in an arm, hand, or leg

numbness on one side of the body

sudden dimness or loss of vision, particularly in one eye

sudden difficulty speaking

inability to understand what someone is saying

dizziness or loss of balance

sudden, lasting, excruciating headache.

It is difficult to overemphasize the importance of identifying and treating a stroke as soon as possible. Warning signs can begin anywhere from a few minutes to days before a stroke (see “Stroke warning signs and symptoms,” above). In a Gallup survey, 97% of people over age 50 did not recognize the warning signs of a stroke. Everyone, especially those who are at increased risk for stroke, should learn these warning signs and know what to do if they occur. The National Stroke Association has devised the FAST checklist (see “Act FAST”) to help determine whether a person is having a stroke.

ACT FAST If the answer to any of the questions below is yes, there’s a high probability that the person is having a stroke.
Face	Ask the person to smile. Does one side of the face droop?
Arms	Ask the person to raise both arms. Does one arm drift downward?
Speech	Ask the person to repeat a simple sentence. Are the words slurred? Does he or she fail to repeat the sentence correctly?
Time	If the answer to any of these questions is yes, time is important. Call 911 or get to the hospital fast. Brain cells are dying.

When stroke symptoms occur, quick action is vital. If you think you or someone with you is having a stroke or transient ischemic attack (TIA), call 911. You should be taken to a hospital emergency room, preferably one that specializes in treating stroke as it occurs (called acute stroke). If you know you are at risk for stroke, find out ahead of time the name and location of the nearest hospital that specializes in treating acute stroke.

Since the 1980s, researchers have developed rapid, safe, and effective diagnostic techniques that accurately identify the extent and location of a stroke and the nature of the blood vessel (vascular) problem causing it. The goal of treatment is to restore blood circulation before brain tissue dies. The time frame for reaching this goal is frighteningly slim. To prevent brain cell death that is significant enough to cause disability, treatment is most effective if it starts within 60 minutes of the onset of symptoms.

One of the main clot-dissolving drugs, recombinant tissue-plasminogen activator (tPA), must be given within three hours of the start of stroke symptoms, but earlier is better. An important goal of research is to find treatments that can buy time by protecting the patient’s brain until blood circulation is restored, thus improving the odds of survival and decreasing disability.

LUNG CANCER

Lung cancer is usually discovered late when it’s difficult to treat and has often spread outside the lung. A reliable screening test to find it at an earlier, more treatable stage would be a legitimate breakthrough—and could potentially save thousands of lives. About 160,000 Americans die each year from lung cancer, which is more than who die from  breast, prostate and colon cancer combined. Chest x-rays do a good job of finding small lung cancers that can be removed surgically. Why not use them to screen for lung cancer? Because at least a half-dozen studies have been done and for reasons that aren’t entirely clear, early detection with chest x-rays hasn’t translated into prevention of fewer deaths from lung cancer. And in screening, early detection is a means to an end. The real goal is preventing deaths from the disease that is being screened for (and deaths in general).

So it was big news today when the National Cancer Institute announced today that a large study sponsored by the institute showed that screening current and former heavy smokers with computed tomography (CT) scans did, in fact, reduce the risk of dying from lung cancer by 20% compared with screening them with chest x-rays. Moreover, those who were screened with CT scans were 7% less likely to die from any cause during the study’s five-year follow-up period.

Good news, and a long time coming for those who have watched disappointing findings from the chest x-ray studies pile up.

But if today was first time that most of us heard about the National Lung Screening Trial, it probably wouldn’t be the last. It’s almost certainly going to stir up more than its fair share of controversy.

Here are a few of the hot buttons:

• The NCI says there are more than 94 million current and former smokers in the United States (mind you, not all of them are heavy smokers, so the population to be screened may be smaller). It will be very expensive to screen them all with CT scans. How much a screening CT of the lung will cost is hard to say, especially if they become routine, but the NCI says the current Medicare reimbursement rate for a diagnostic CT scan of the lung is $300.
• Some may argue that smokers shouldn’t be entitled to such an expensive test—or should have to shoulder a large share of the cost. The counterargument is why single out smokers when other bad health habits result in expensive tests and treatments.
• The NCI itself showed that there’s concern that some people may see an effective screening test as a reason to tune out the dire health warnings about tobacco and cigarettes. In a Q&A about the study  posted on its Web site today (which is well worth reading if you want more detail about the study), the third question is, “Is it OK to keep smoking because there is a screening test that has benefit?” The answer begins with an emphatic, “No.” It’s hard to imagine that people would actually ask such question, but the NCI apparently was worried enough to pose it.
• Radiation exposure and the cancer risk from medical imaging (and CT scans in particular) has become a major issue. Will the radiation from CT screening for lung cancers add to the problem? The NCI position: the radiation from a screening CT is far less than the dose from a diagnostic one and that benefit of finding and treating early lung cancer will likely outweigh the risk from a low dose of radiation from CT scanning.
• In the Q&A about the study, the NCI says that between 20% and 60% of  screening CT scans of current and former smokers show some kind of abnormality and that most are not lung cancer. CT scanning for lung cancer could generate a large number of false positives: results that indicate the possibility of cancer but turn out not to be. False positives result in worry and additional tests, which in the case of lung cancer would include invasive biopsies.

Of course many of our current screening tests for cancer have shortcomings, cost plenty, and are controversial. The debates about the value of mammography never seem to end. Yet we get behind screening tests for a whole variety of reasons, not the least of which is that cancer caught late is so lethal and, these days, astronomically expensive to treat.

ALCOHOLIC LIVER DISEASE

In the last 15 yr, UK alcohol-related deaths have doubled. In 2005, there were 8386 deaths related to alcohol. Death rates in both sexes and all age groups are increasing. Alcohol-related deaths are twice as frequent in males.This review aims to highlight the different subtypes of alcoholic liver disease (ALD) and discuss the management of the various ways in which ALD can present to the intensivist.

ALD is conventionally divided up into three histological types, although features of each may coexist in the same patient.
Steatosis
The metabolism of ethanol causes the accumulation of lipid in liver cells. This is steatosis, or 'fatty liver', estimated to occur in 90–100% of all heavy drinkers.Largely symptom free, it resolves completely within a few months of cessation of alcohol intake.
ALCOHOLIC  HEPATITIS
Ethanol metabolism can generate reactive oxygen species and neo-antigens,promoting inflammation. This 'alcoholic hepatitis' (AH) occurs in 10–35% of heavy drinkers. It may be mild and virtually asymptomatic or it may lead to acute flare ups with all of the signs of the systemic inflammatory response syndrome (SIRS) and subsequent multi-organ failure (MOF). In patients with confirmed AH on biopsy who continue to drink, 40% progress on to cirrhosis.
CIRRHOSIS
Prolonged hepatocellular damage generates myofibroblast-like cells which produce collagen resulting in fibrosis. As hepatocytes are destroyed and liver architecture changes, hepatic function falls and increased resistance to portal blood flow produces portal hypertension. Approximately 8–20% of heavy drinkers will develop cirrhosis, which may be asymptomatic. However, acute episodes of liver failure may be induced by episodes of AH or complications of portal hypertension such as variceal bleeding. In patients whose first presentation is an episode of severe decompensated ALD, 85% will have AH and more than 70% will have cirrhosis.
The single biggest risk factor is the quantity of alcohol ingested, irrespective of what form it is taken in. There is considerable debate as to what constitutes a 'safe' level of alcohol consumption, although it is evident that females are more at risk than males at any individual consumption level. Epidemiological data had initially suggested consumption of 80 g of ethanol per day in men and 60 g in women, for between 10 and 12 yr, is necessary for alcoholic liver damage to occur. However, recently these levels have been questioned, with new figures of 40 g per day in men and 10–20 g per day in women being associated with an increased relative risk of developing liver disease. For comparison, one UK 'unit' of alcohol contains 10–12 g of ethanol.
Other risk factors include obesity and hepatitis C infection. Despite this, it is unknown exactly why ALD only affects a proportion of heavy drinkers, even in the presence of other risk factors.
Patients with ALD may present to the intensive care unit (ICU) with one of the 'acute on chronic' complications of cirrhosis such as encephalopathy or variceal bleeding. Alternatively, they may present with an episode of severe hepatitis which may progress on to MOF. As patients with AH may have coexistent cirrhosis, this group can present with features of both acute and chronic liver disease.
HISTORY
Features in the history include high alcohol intake, history of alcohol abuse, history of alcohol-related diseases (e.g. pancreatitis), and accidents. Additionally, certain jobs (e.g. a publican) increase the likelihood of heavy drinking. In patients in whom dishonesty is suspected, a more accurate alcohol history may be obtained from the family.
EXAMINATION
Although alcoholic patients may have no abnormal examination findings when well, on presentation to ICU, they will have signs of either acute hepatitis, chronic liver disease, or both . In addition to these, there are specific features that should be looked for:

assessment of airway stability;

       signs of chest infection or aspiration at auscultation;

signs of SIRS (pulse, arterial pressure, temperature, etc.);

  assessment of fluid status;

  assessment of GCS and level of encephalopathy;

  assessment for signs of gastrointestinal (GI) bleeding (pallor, melaena on PR   examination);

  examination of input/output charts;

        bowel charts

INVESTIGATIONS
Common investigations requested on patients with ALD are listed in Individual tests are discussed under the different diagnoses subheadings.
GENERAL MANAGEMENT
General supportive care should be instigated in a patient with ALD, irrespective of presentation. Oxygen via a face mask or nasal specs should be commenced, large-bore i.v. access obtained, blood tests taken , and fluid resuscitation commenced. Regular glucose measurements should be taken. Disordered coagulation should only be treated if bleeding has occurred or invasive procedures are planned. Urine output should be closely monitored and oliguria should be aggressively treated. Care should be taken not to rapidly correct severe hyponatraemia which may exist in long-standing cirrhotics due to excess anti-diuretic hormone secretion. However, sodium-containing fluids are not specifically contraindicated in the alcoholic patient in the acute setting as hypotensive organ failure is likely to be more dangerous in this situation than the long-standing sodium retention. Hypokalaemia is also common and should be treated with careful supplementation.
Medications which may provoke hypotension, encephalopathy, or renal dysfunction [diuretics, angiotensin-converting enzyme inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), sedatives, etc.] should be stopped. An appropriate withdrawal regime and ulcer prophylaxis should be started along with vitamin supplementation. Thiamine should be given i.v. before glucose-containing compounds. Suitable antibiotics are required if any infection is suspected. Additionally, prophylactic antibiotics should be started in patients with bleeding.
Nutrition should be commenced early. Malnutrition is common in alcoholic patients and is associated with severity of liver dysfunction and poor outcome. Enteral feeding is preferred over i.v. feeding, and standard feeds can be used. Protein restriction is no longer recommended due to the risk of muscle wasting; however, if encephalopathy supervenes or worsens, then branched chain amino acid feeds should be considered.

Signs of acute hepatitis Jaundice Tender hepatomegaly Fever (<38.50, often sawtooth) Signs of chronic liver disease Leuconychia Palmar erythema Dupytren's contracture Spider naevi Telangactasia Bruising Oedema (hypoalbuminaemia) Parotid swelling Gynaecomastia Hepatomegaly Testicular atrophy Encephalopathy Portal hypertension Ascites Splenomegaly Caput medusae (abdominal varices) Poor nutrition Muscle wasting (back of hands) Weight loss/cachexia Glossitis

 

Blood tests FBC Clotting U+E LFT Other electrolytes (magnesium, calcium, phosphate, etc.) Glucose Group and save/XM Blood cultures Imaging CXR Abdominal ultrasound Other investigations Urine dipstick MSU Diagnostic abdominal paracentesis (if ascites present) Other investigations often indicated Amylase (suspected pancreatitis) Ammonia (encephalopathy) Intra-abdominal pressure (IAP) (hepatorenal syndrome, HRS) Renal tract ultrasound (deteriorating renal function to rule out obstruction) Abdominal CT (suspected perforation) Head CT (encephalopathy, sepsis)
Modified discriminant function (mDF) = Bilirubin (mg dl−1) + [4.6×prolongation of PTT above control (s)] Note: convert bilirubin in micromoles per litre to milligrams per decilitre by dividing by 17.1. Model for end-stage liver disease (MELD) = 3.8×loge bilirubin (mg dl−1) + 11.2×loge INR + 9.6×loge creatinine (mg dl−1) Note: maximum score is 40; values of <1 are given values of 1; recent dialysis requires a creatinine value of 4.0
Child–Pugh score
Criterion	1 point	2 points	3 points
Bilirubin (mmol litre−1)	<34	34–50	>50
Albumin (g litre−1)	>35	28–35	<28
INR	<1.7	1.7–2.2	>2.2
Ascites	None	Controlled	Refractory
Encephalopathy	None	I–II or controlled	III–IV or refractory
Note: Scores 5–6=class A; Scores 7–9=class B; Scores 10–15=class C
Glasgow AH score
Criterion	1 point	2 points	3 points
Age	<50	≥50	—
WCC (109 litre)	<15	≥15	—
Urea (mmol litre)	<5	≥5	—
PT ratio	<1.5	1.5–2.0	>2.0
Bilirubin (mmol litre−1)	<125	125–250	>250
Note: Scores of 9 or above have a >50% 28 day mortality

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