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Member since Jun-04-08 · Last seen Apr-21-15
Good Day to All! Ma-ayong adlaw sa tanan. And my thanks to for this excellent website. Salamat Opinions:

1. World Chess Championship

The true Chess World Champions are the holders of the Traditional Title that originated with Steinitz & passed on in faithful succession to Lasker, Capablanca, Alekhine, Euwe, Botvinnik, Smyslov, Tal, Petrosian, Spassky, Fischer, Karpov, Kasparov, Kramnik, Anand, and Carlsen. The sacredness of this Title is what makes it so valuable.

And how does one become the true Chess World Champion? In general, by beating the previous Titleholder one on one in a Match! Matches are preferred over Tournaments because of the Tradition of the WC Succession & because the chance for pre-arranging a Tournament result is more likely. The only exceptions to this rule:

A. In case where the Candidates and World Champion participate in an event that all the participants agree to be a World Championship event because of extraordinary circumstances.

Thus, the 1948 World Championship Tournament was justifiable because of the death of the Title holder Alekhine.

Likewise, the 2007 WC Tournament was justifiable under the extraordinary circumstances of the Chessworld trying to heal its internal rift over the 1993 Kasparov Schism. Anand himself became the World Champion in this 2007 Tournament & not in 2000 when he won a knock-out FIDE Tournament. Caveat: Some chess fans deem the 2007 WC Tournament as illegitimate, considering that Anand became the World Champion only in 2008, when he beat the previous Titleholder Kramnik in a WC match. From this perspective Anand only became the Undisputed World Champion in 2008.

Karpov lost his Title to Kasparov in 1985, & never regained it in the 1990s events that FIDE labeled as 'world championships'. All solely FIDE Champions that emerged outside WC Traditional Succession elaborated on above, strong as they were, were not true World Champions (eg., Bogolyubov 1928, Khalifman 1999, Ponomariov 2002, Kasimdzhanov 2004, Topalov 2005).//

B. In case the previous Titleholder defaults an event that the Chessworld largely deems as a World Championship event in the Tradition of the World Championship Succession. Thus, Karpov was the true successor to Fischer who defaulted their WC Match in 1975.

2. The strongest chess events in different eras of chess history?

Because of the brain's limitations explained below, the best professional (amateurs don't matter much in top level chess) chess players of each generation beginning in the Lasker era have always played at a similar level - near the maximum allowed by human standards. Now there are larger cohorts of chess professionals post WW2 than preWW2 thanks to government state funding in the Soviet era and presently corporate funding. The result is that large preWW2 tournaments had numerous 'bunnies', relatively weak players. By the Kasparov era, super-tournaments that featured most of the top ten, and no bunnies, had became more common. However, the top 4 or 5 since Lasker's time have always been very strong.

Consequently the smaller the top-player-only tournament, the stronger it gets. For any era. If there was a double round robin tournament in 1914 featuring Lasker, Capablanca, Alekhine, and Rubinstein, and no other, it would be as strong as any present day super-tournament.

Now weed out everyone except the two strongest players in the world. What we (usually) get is the chess World Championship match.

There has been talk of elite tournaments, composed only of the strongest top masters and no weaker bunnies replacing the World Championship match in prestige, probably because of the assumption that they would be the strongest chess events possible. False assumption. The strongest chess events in chess history generally have been World Championship matches. Even the strongest masters in each generation usually do not match the world champion and challenger in chess strength. In a World Championship match, the contestant has to meet the monster champion or challenger over and over again, with no weaker master in between. Capablanca vs Lasker 1921 was just as strong a chess event as the recent Carlsen vs Anand 2013, and far stronger than Zurich 2014. (Imagine having to play 14 straight games with a computer-like errorless Capablanca at his peak.)

3. The strongest chess players in chess history?

IMO the 1919 version of Capablanca & the 1971 version of Fischer, both of whom played practically error-free chess, are it; updated in opening theory, they should beat anyone in a match.

If computers were self-aware, I have no doubt that they would unanimously choose the 1916 to 1924 Capablanca as the strongest chess player in history. And please no red herring remark that Capa played only 'simple' chess. This young Capablanca played some of the most complicated, sharp, double edged, and bizarre positions possible; and played them without making a single losing error (and by all accounts with unsurpassed quickness), something that has always befuddled my mind when I got to peruse through his games.

We have to take this question in the context of the limits of the human Anatomy and Physiology. A concrete example would be the one hundred meter dash. The human body is designed such that the limit it can run is about 9 seconds. In order for a human being to run faster, we would have to redesign the human anatomy into that of say a cheetah. One can rev up the human Anatomy and Physiology, say with steroids, but this regimen would hit an eventual Stonewall too; the same way that we could rev up human proficiency to learn openings with computer assistance.

Since the Nervous System has physiological limits (example of a limit- neuronal action potential speed don't go up much more than 100 m/s) and so limits the human chess playing ability, increasing the number human chess players, thus expanding the normal curve of players, simply creates more possibilities of players playing like a Fischer in his prime, but will not create a mental superman who plays chess at computer levels. This explains why human and computer analysis indicate that Lasker was playing on a qualitatively similar level as more recent WCs.

'Worse' in chess, any computer assistance ends once the opening is over. After a computer-assisted opening prep, every GM today has to play the game the way Lasker did a hundred years ago, relying on himself alone, with the same fundamental chess rules and chess clock. An Encyclopedic opening repertoire is not a necessity to be a top player. In fact, there are World Champions who did not do deep opening prep; they just played quiet but sound openings that got them into playable middlegames and then beat their opponents in the midlegame or endgame. Just look at Capablanca, Spassky, Karpov, and now Carlsen.

Because of subconscious adherence to the narcissistic generation syndrome, the belief that everything that is the best can only exist in the here and now, many kibitzers would not agree to the above theses. While it is true that there have been more active chess professionals and consequently larger cohorts of top chess masters on a yearly basis since WW2 thanks to Soviet state funding and present corporate funding, the very top chess masters since Lasker's time have always played at a similar level- within the limits imposed by the human brain. There is no physical law that bars a pre-WW2 chess master from playing chess as well as today's generation. The human brain has not changed in any fundamental manner in the past tens of thousands of years.

4. The greatest chess players in history?

A related question is who is the greatest chess player in history. The answer depends on the criteria one uses. Since I place great emphasis on the ability to play world class chess for the longest period of time, Lasker would be it. He was playing at peak form from 1890 age 22 (when he began a remarkable run of match victories over Bird, Mieses, Blackburne, Showalter, and culminating in his two massacres of Steinitz) until 1925 at age 57 (when he nearly won Moscow after winning new York 1924). Kasparov (high plateau from 1980 to 2005) and Karpov (high plateau from 1972 to 1996) would follow. (At their very peak though, I believe that Kasparov was stronger than Karpov, and both were stronger than Lasker; and the peak Capablanca and Fischer were stronger than any of them.)

5. Computers vs Humans, who is stronger?

Another related question is how history's top masters would fare against computers. It's obvious from Kasparov's time that computers would totally crush them all. Opening knowledge would not matter much. Computers swamp human opponents in the middle game, simply by calculating more variations more rapidly by several orders of magnitude. Peak Capablanca probably would have the best score among humans. Talk about another level of playing is fans' subjective and IMO wrong words for their favorite players, unless one talks about chess computers. Chess computers do play at a higher level.

6. On the game and chess players young and old, past and present:

The proposition that an older player would not be able to adjust to the openings and methods of a younger generation is false, as evidenced by the observation of strong masters whose careers happened to span generations beating the tar out of weaker masters of the next generations. Lasker provides a classic example; he was beating Mieses, Blackburne, and Steinitz in the 1890s, and crushing masters versed in the hyper-modern teaching of controlling the center indirectly- Reti, Bogolyubov, and Euwe in the 1920s. In more recent times, we have Victor the Terrible, who learned most of his chess in the 1940s and 1950s, whom we have seen competing successfully with the so-called computer generation even at an advanced age.

The notion that computers are more advantageous to younger players IMO is not quite right. Younger players should have more energy and stamina in studying chess openings and endgames for long hours everyday compared to older players without computers, but the use of computers would tend to make the learning process easier for every one including the older ones.

As a corollary, computers also make it easier today for very young players in their early teens to peak at a younger age than in past eras, although they tend to level off in their early 20s to their high plateau, defined by their inborn talents and determination.

In brief. computers tend to level chess learning for everyone, young and old.

This is not a rigid rule. The best games I have ever seen played by a 12-13 year old are Capablanca's; and Tal, Karpov, and Kasparov reached their high plateau in their early 20s in a computer-less era, similar to computer age Carlsen. However let it be noted that Carlsen reached his peak sidestepping intensive computer-prepped tactical openings and beating his competitors in the old fashioned way in the middlegame and endgame. These masters peaked early not because of computers by because of their immense chess talent. Perhaps normal rules do not apply to these geniuses.

Another false notion is that the nature of the middlegame today is somehow different from the middlegame in the past. The easiest way to prove the wrongness of this proposition is by observing CG's daily puzzles. Do not peek at the names of the players that played these puzzles, and don't look at the dates. Can you glean from the middlegame play and combinations in the puzzles the date they were played? You can't. You would not know if it was played in 2014, 2000, 1950, or 1900. Chess combinations don't just suddenly change their stripes just because a hundred years have passed.

Another observation is that when the best masters of the past, Lasker and Capablanca met the occasional 'modern' structures of the Sicilian Scheveningen and Dragon, KID, Modern Benoni, Benko Gambit, they played strategically perfectly, in just the way these opening structures should be played. So how did these masters play openings and the resulting middlegame structures that are deemed incomprehensible to them by some of today's dogmatically 'modern' kibitzers? The answer is that chess rules and principles have not changed. Center, rapid development, open files and diagonals, holes, weak pawns, piece activity, initiative and attack, positional sacrifices and all types of combinations were as familiar to them as to us.

Instead, it is the frequencies of a few middlegame pawn structures have changed since WW2. Not the Ruy Lopez or QGD, but obviously Sicilians and KIDs are much more common post-WW2. Since so many games nowadays begin with the Sicilian and KID, people associate these with being 'modern' (which is a rather vague undefined term IMO). But certainly Lasker and Capablanca understood the middlegame principles behind them and when they did get these positions they played them excellently, like the top masters they are.

Moreover, Keres is a smoking gun, bomb proof evidence of the fallacy of Watson's speculation that pre-WW2 masters would not be able to learn 'modern' chess, and Larsen's assertion that he would crush everyone in the 1930s. The glaring fact is that Keres is a 1930s pre-WW2 master whose career extended up to the 1970s, and he did learn (and contributed) to the newer opening variations (the most famous of which is the Keres attack which he invented in 1943). Tellingly enough Keres beat both Watson and Larsen.

7. On ratings:

Elo ratings reflect relative and not absolute chess strength.

Chessplayers are naturally arranged in populations partitioned by geopolitical regions & time periods that have infrequent contacts with one another. Within such a population, players get to play each other more frequently, thus forming a quasi-equilibrium group wherein individual ratings would tend to equilibrate quickly; but not with outside groups. With caveats & in the proper context, FIDE/Elo ratings are simply fallible descriptors & predictors of an active player's near-past & near-future performances against other rated players, & only within the same quasi-equilibrium group.

As corollaries: the best way to evaluate a player's strength is to analyze his games & not his ratings; one cannot use ratings to accurately compare the quality of play of players from the past and present, or even the same player say a decade ago and today; & care should be taken in the use of ratings as a criterion in choosing which players to seed into the upper levels of the WC cycle. All the above often entail comparisons between players from different quasi-equilibrium groups separated by space and/or time.

Regarding inflation deniers, they imply that Elo ratings reflect absolute and not relative chess strength. Professor Elo himself would condemn their view. If the top 20 players were to suffer a serious brain injury and begin playing like patzers, but play no one else for the next decade, they would more or less retain their 2700s ratings, although they would be playing terrible patzerish chess.

8. Best Qualifiers?

The credible, fair, tried & tested Zonals - Interzonals - Candidates (with known strong players directly seeded into the Interzonals & Candidates; & here ratings may be used with caveats) over the random World Cup and the elitist Grand Prix. If possible long Candidate matches and 16 to 24 game World Championship matches. However, with the passing of the state-funded chess era of Soviet times, I begin to doubt if the strict money guzzling qualification process above can be re-installed.

9. The 1993 Chess Rift and Kramnik:

Regarding the Rift in the chessworld after Kasparov split in 1993, I believe that Kramnik has done more than any other individual in helping heal it by concrete actions - agreeing to a WC Match with Topalov in 2006 & not walking out when he could have done so with the support of most of the world's top GMs after getting accused of cheating; & agreeing to Defend his Title in a WC Tournament in 2007, the first time a living Titleholder has agreed to do so in chess history. My eternal gratitude to him.

10. Finances of a would-be Challenger:

Regarding all kinds of problems chessplayers outside of Europe & the USA face in their quest for the Title, Capablanca & Anand have proven it's possible for a non-European non-USA chessplayer to be World Champion; but apparently only if you have the chess talent of a Capablanca or Anand! For others, I guess they would have to try to get monetary support & good seconds somewhere to have some hope for a Title shot.

11. Ducking a World Championship re-match:

Alekhine vs. Capablanca - Not definitively resolved. If pushed, I would tend to favor Capablanca given that pre-WW 2, there was no definitive cycle to choose the Challenger &, after all is said and done, it was the Champion who set the conditions & who chose his Challenger. AAA could & should have chosen Capa; & there was ample time, more than a decade, to do so before WW2. On the other hand, Capa's pride may have caused him to behave arrogantly & thus offend AAA. The issue is very much debatable. //

Kramnik vs. Kasparov - For me, it's resolved. Kudos to Kramnik for trying his best to install a decent Qualifying Event. Kasparov for his reasons clearly did not want to go through the Qualifying Event that he himself had pledged before losing his Title; & did not even seem serious in playing the solely FIDE champions. Why? I can only speculate that Kasparov would rather retire than risk a loss in a Qualifier or a match to either a FIDE champion or to Kramnik. If he regained his Title, he would be the greatest Champion in history, but there was risk involved. If he retired, he would still be the greatest Champion in history, but there would be no risk involved. Kasparov chose the latter & no one should blame him for that decision; & more so don't blame Kramnik!

12. Predictions for Hypothetical World Championship Matches:

Lasker vs. Pillsbury, Rubinstein, Maroczy - Lasker wins 2, loses 1 match //

Lasker vs. Capablanca (inexperienced) 1914 - Lasker close win //

Capablanca (not overconfident & not having TIAs) 1929 to 1937 vs. Alekhine or any other master - Capa win //

Alekhine (sober & prepared) vs. Capablanca (w/ severe HPN & numerous past strokes), Botvinnik, Keres, Fine, Reshevsky, Flohr 1939 - Alekhine win //

Alekhine (alcoholic, ill, & depressed) vs. Botvinnik 1946 - Botvinnik win //

Fischer (inactive for 3 years) vs. Karpov 1975 - Karpov win//

Kasparov vs. Shirov 2000 - Kasparov win. (But GKK should still have given it to Shirov. And don't blame Kramnik. Had Kramnik declined, GKK would have chosen another; & Shirov would still be frustrated.)


I have opened a <'multi-experimental' forum> below. Its nature is that of several secret social and psychological experiments, whose objectives and parameters, and the rules that follow, are strictly defined and which I may or may not reveal. Readers of this forum might be able to deduce some of these rules. Accordingly messages shall be retained or removed with or without explanation, even those from my dear friends here in CG, although I am making it clear here that absolutely no offense is intended to any one in this experiment. I may or may not respond to certain questions and messages, also according to the rules. To my friends: Please bear with me in this matter. There can be a certain amount of disinformation and propaganda in the messages that are retained.

The title of this <'multi-experimental' forum> is:

Biased Journal of a Fourth World Brain Operator

Some abbreviations

CiH = the public City Hospital

PrvH = Private Hospital. There are three main ones. So PrvH 1, PrvH 2, PrvH 3.

ProvH = the public Provincial Hospital

SOL = Space Occupying Lesion

SQ = Subcutaneous tissue layer of the skin or scalp

CVA = Cerebrovascular accident = stroke

EDH = Epidural Hematoma, blood above the dura mater, the outer covering of the brain, and beneath the skull.

SDH = Subdural Hematoma, blood beneath the dura mater.

ASDH = Acute Subdural Hematoma, SDH incurred recently, usually less than a week

CSDH = Chronic Subdural Hematoma, SDH that is more than two weeks old

HCP = Hydrocephalus, too much CSF in the brain's ventricular system

CSF = Cerebrospinal Fluid

CNS = Central Nervous System

CAB = Continuous ambubagging

ETT = Endotracheal tube (for airway purposes)

NGT = Nasogastric tube (for feeding purposes)

NOD = Nurse on duty

The Oracle = personification of the CT (computed tomography) scan.

Magic mirror = the computer monitor where one can see CT scan images.

Witching Hour Admissions or Referrals = 12 midnight to 5am

MF = Motorcycle Fall

Craniectomy = neurosurgical procedure that involves removing a portion of the skull

Tracheostomy = a surgical procedure to create an opening through the neck into the trachea (windpipe)

INTUBATE: To put a tube in, commonly used to refer to the insertion of a breathing tube into the trachea for mechanical ventilation

EXTUBATION: the removal of a tube especially from the larynx after intubationócalled also detubation.

Uneventful day = Most likely still a busy day, making daily rounds in the hospitals, following up post-op patients, seeing patients in the OPD, answering referrals, admitting all kinds of patients in the hospitals; nevertheless a day in which nothing interesting has caught my attention.

>> Click here to see visayanbraindoctor's game collections. Full Member

   visayanbraindoctor has kibitzed 7168 times to chessgames   [more...]
   Apr-20-15 W So vs Akobian, 2015 (replies)
visayanbraindoctor: <Other times I see ads for Filipino women.> Apparently anytime anyone anywhere in the world opens up into the internet, there is a likely chance of seeing an ad for Filipinas (?). That's mildly troubling. As a chess player, I would not have complained. But I guess ...
   Apr-20-15 W So vs R Mamedov, 2015 (replies)
visayanbraindoctor: <cro777: 14...Qa5?> You're right. Later after 18. fg6 fg6 19. e5! de5 20. Be5 IMO So had a positionally won game. Mobile queenside pawn majority, good central control, weak isolated Black e-pawn. So simplified straight into the winning endgame here when he had the ...
   Apr-20-15 visayanbraindoctor chessforum
visayanbraindoctor: 20 April 2015. <18 April 2015. About 10:30 pm. An SUV driven by a drunk hit a tricycle, and on top of them a motorcycle landed. I had to intubate the comatose driver of the motorcycle 30M.> There was a delay because of financial reasons. 30M was intubated in PrH1, ...
   Mar-26-15 twinlark chessforum (replies)
   Mar-10-15 Annie K. chessforum (replies)
visayanbraindoctor: Regarding the salps mentioned in https://whyevolutionistrue.wordpres... Salps and other tunicates fascinate me. They exhibit 1. a hollow central nervous system that develops as an inpouching of the dorsal ectoderm, exactly the same as humans. In fact they are classified ...
   Mar-06-15 Karpov - Fischer World Championship Match (1975) (replies)
visayanbraindoctor: <Lambda: <Fischer-Karpov is, outside of Alekhine-Capa II, the most lamentable missing match in the history of our game.> I'm not sure why Alekhine-Capa II should be such a priority, we have one perfectly good match between the two already. As well as ...
   Mar-04-15 Zurich Chess Challenge (Rapid) (2015)
visayanbraindoctor: <RookFile: Personally, I think that rapid games are good for a few laughs, but little else.> I think that the best quick game chess players in history were Capablanca and Fischer. Yet Fischer had nothing much to say about the seriousness of quick games, and ...
   Feb-11-15 GRENKE Chess Classic (2015) (replies)
visayanbraindoctor: <1d410> I have also played in competitions of course if that's your next question. I will answer in more detail in my forum, just click at my name.
(replies) indicates a reply to the comment.

Kibitzer's Corner
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Premium Chessgames Member
  visayanbraindoctor: 22 March 2015. Entry 1. Just before midnight, a Pulmonologist called me to PrH2 ER. He had come across a group of Catholic priests that he knew and that were bringing in an unconscious deacon who had fallen off a motorcycle. I had a CT scan done ASAP. It showed bihemisphere acute subdural hematomas, a right temporo-petrous fracture with underlying temporal lobe hemorrhagic contusion and a small epidural hematoma.

I told the Monsignor who accompanied him that I was advising an operation. The senior priest was still hesitant, and the Pulmonologist suddenly told him that time was of the essence that his deacon had to be operated on right now. Shortly after, the deacon's sister-in-law, whom the Monsignor had called, arrived and gave the consent.

So I rushed the patient from ER direct to OR and operated on both sides of his head. (Right temporo-fronto-parietal craniectomy, evacuation of acute subdural hematoma, left temporo-fronto-parietal craniectomy, evacuation of acute subdural hematoma, bones transplant to left hemiabdomen subcutaneous layer, 3/22/15 2:10 to 3:40 am.)

Premium Chessgames Member
  Annie K.: You'd think that poor blind man had enough bad luck already... :(

<<Annie K.:The details about bone replacement always interest me too. :)> Unfortunately I am the wrong guy to ask because I don't do this. I prefer putting back the bone itself. Essentially however, it consists of placing a titanium plate on the skull defect and screwing it to the adjacent bone with titanium screws.>

I think your solution is the better one, personally. :) The idea of the patients spending the rest of their lives walking around with sharp pieces of metal in their heads does not strike me as a great idea, however expensive those may be. :s

Premium Chessgames Member
  Annie K.: Your reason for the general phenomenon of fluids circulation sounds very sensible. :) It has always been my impression that cleansing the body of toxins and bacteria, as well as supplying it with oxygen and nutrients, was the function of the blood and other fluids.

But circulation is one thing, production is another - I was wondering about the production of CSF: if that much is produced per day, to maintain equilibrium, that much must also be lost / disposed of / secreted per day. Where does it go? Are other bodily fluids also produced at this rate? IIRC, blood is cleansed by passing through the kidneys, so it's more of a reusable resource.

Premium Chessgames Member
  visayanbraindoctor: <Annie K.: You'd think that poor blind man had enough bad luck already> He was born with no eyes. I suspect many of them don't get to be as active as most of us, and live a mostly sedentary lifestyle. That would make them more prone to cardio and cerebro vascular diseases.

<production is another - I was wondering about the production of CSF: if that much is produced per day> Slightly more than half a liter per day. A tissue called the choroid plexus produces it in the brain's ventricles.

<Where does it go?> It circulates around the brain through the ventricular system, into the subarachnoid space, and gets absorbed in the arachnoid granulations on the sagittal sinus on the brain's midline surface.

<Are other bodily fluids also produced at this rate?> Now that you mention it, I don't think any other type of body fluid gets produced and secreted out of specific compartment at this rate, except understandably enough urine. If we would drink 7.2 liters of water per day, all of it will get produced at the beginning of the urinary tract and get excreted out of the body in a day, and an average rate of 300 cc per hour. The minimum urine output of healthy person is 30 cc per hour, or slightly more than 0.7 liters a day. Less than that is indicative of kidney failure.

Premium Chessgames Member
  visayanbraindoctor: 23 March 2015. Entry 1.

<22 March 2015. Entry 1. Just before midnight, a Pulmonologist called me to PrH2 ER. He had come across a group of Catholic priests that he knew and that were bringing in an unconscious deacon>

I made rounds early on 35M, the deacon I operated on yesterday. <I told the Monsignor who accompanied him that I was advising an operation.> I caught the Monsignor inside the ICU just finishing extreme unction on the patient. Since the previously comatose 35M could now follow commands, I told the Monsignor I don't think 35M would die.

Premium Chessgames Member
  visayanbraindoctor: 25 March 2015. Entry 1. I made a terrible blunder, fatal for my patient, 16M a MF victim. I failed to intubate him on time. Depressing for me, horrible for his father and sister who were with him, and terminal for my patient. (One of the cases I don't want to talk about much.)
Premium Chessgames Member
  visayanbraindoctor: 27 March 2015. Entry 1. An anisocoric (left pupil 4 mm, right 2mm) comatose (GCS 3, no reaction to pain at all), hypotensive (BP 80/60) MF victim 38M arrived in PrH1 ER from a neighboring province. CT scan showed a large 70cc epidural hematoma underneath a a depressed left frontal bone fracture. His low BP is explainable by a femoral fracture (a patient can bleed to death from these fractures). With a herniating patient I had no choice but to do a direct to OR order, in the meantime pumping him with a 1 liter of a plasma volume expander. By the time the patient reached the OR both his pupils were dilated. I decided to proceed hoping his brain was not yet infarcted. The massive blood loss he had incurred due to the femoral fracture deranged the clotting mechanism of his blood, and I had to tightly and circumferentially tack the dura after evacuating the EDH, in order to lessen the bleeding. The Anesthesiologist infused 2 more liters of volume expander. I had completed the operation by the time the blood arrived. (Right fronto-temporo-parietal craniectomy, evacuation of epidural hematoma, bone transplant to left hemiabdomen subcutaneous layer, 3/27/15 4:40 to 5:48 pm.)

Post-op, his left right pupil began contracting. However, I do not think he will survive. His left pupil is still dilated, and during the operation, I noted that his brain was not pulsating, a sign of an infarcted brain.

Premium Chessgames Member
  visayanbraindoctor: 29 March 2015. Entry 1. <27 March 2015. Entry 1. An anisocoric (left pupil 4 mm, right 2mm) comatose (GCS 3, no reaction to pain at all), hypotensive (BP 80/60) MF victim 38M>

Both of 38M's pupils have dilated, and he is now brain dead.

Premium Chessgames Member
  visayanbraindoctor: 31 March 2015. Entry 1. I intubated 61M in CiH just as he was gasping his life away. He had fallen down the stairs of his house while drunk, and incurred a complete C4 (cervical 4 level, at the neck) spinal cord transection. He was already severely aspirated. Right after intubation, he went on CP arrest, but I managed to revive him with CPR and epinephrine. He was comatose, with low BP. I told his grieving daughters that their father most likely only had a day or two to live.
Premium Chessgames Member
  visayanbraindoctor: 1 April 2015. Entry 1. <I intubated 61M in CiH> 61M died.
Premium Chessgames Member
  visayanbraindoctor: 2 April 2015.

Entry 1. In PrH1, the Neurologist had referred 64F yesterday specifically for a tube ventriculostomy. 64F has a ruptured ACOM aneurysm. (I can tell from the characteristic CT scan picture.) As is usual in such cases, blood has seeped into her subarachnoid space, and into her ventricles, subsequently causing communicating hydrocephalus. That was several days ago. The patient then deteriorated and the Neurologist had a repeat CT scan done, and this showed an increase in the hydrocephalus. A ruptured aneurysm in a comatose elderly patient carries a very poor prognosis, and I informed 64F's daughter just so. She still insisted on an operation. I proceeded. (Right frontal tube ventriculostomy, evacuation of CSF and intraventricular hemorrhage 4/2/15 3:20 to 3:48 pm.)

The tube ventriculostomy is by itself merely a stopgap; it just prevents the patient from dying outright of hydrocephalus and its complications. My place has no facilities for a proper cerebral angiogram, and the plan would be to send her to a medical center in some other province with such a facility, and ultimately to do a definitive procedure based on the angiogram results, such as coiling. An open craniectomy and clipping of aneurysm operation in this age bracket carries a high morbidity and mortality rate.

Entry 2. After 64F, I operated on 26M, a MF victim. He had arrived in PrH1 ER about midnight. The Oracle revealed a left parietal cerebral hemorrhage underneath an open depressed fracture. The family kept on dilly-dallying on their consent, because some third party wanted them to transfer to another hospital three provinces away. Then 26M began to deteriorate, and a repeat CT scan showed that the hemorrhage had increased and expanded, causing a subfalcial herniation of the cingulate gyrus to the right. I intubated the patient in the ward, and then proceeded to operate. (Left parietal-frontal craniectomy, evacuation of intracerebral hematoma, bone transplant to left hemiabdomen SQ layer 4/2/15 8:55 to 10:21 pm.)

Premium Chessgames Member
  visayanbraindoctor: 3 April 2015.

Entry 1.

At dawn, I was called to PrH1 ER to attend to a comatose (GCS 6) 43M, whose CT scan showed a left basal ganglia hypertensive hemorrhage. It was about 30 cc, yet the patient was deteriorating. He was severely aspirated and I intubated him (with some difficulty because he is short necked and fat, as is typical of such cases). I scheduled him for a tube ventriculostomy operation because the CT scan also showed hydrocephalus, and I thought that he was deteriorating because of that.

The OR called to tell me that the instruments that I had used on 26M last night had not yet been autoclaved, and they had just begun autoclaving. I would have to wait two hours more.

Two hours later: 43M was brought to the OR, but on the way I had a repeat CT scan done. The hemorrhage was now triple its original size. 43M's brain was obviously still actively bleeding.

By the time 43M reached the OR both his pupils were dilated, he had no gag nor corneal reflex, he was totally unresponsive to pain (GCS 3). Nonetheless as he was already on the OR table, I decided to operate. Maybe the situation could still be reversed. (Left fronto-parietal craniectomy, left frontal cortisectomy, evacuation of intracerebral hemorrhage, hemostasis, bone transplant to left hemiabdomen SQ layer 4/3/15 10:45am to 12pm, tracheostomy 12:10pm to 12:20pm. Minimal blood loss, no blood transfusion required.)

Post-op 43M was still GCS 3 and with bilaterally dilated pupils.

Around 12 hours later his BP began to drop. He is brain dead. The operation did not help.

Entry 2.

<2 April 2015. Entry 2. After 64F, I operated on 26M, a MF victim.>

Post-op I did not extubate 26M, just placed him on T-piece with O2 at about 3 liters per minute. The NOD called me in the evening to say that 26M was desaturating. Pulse oximeter showed O2 at 90 and dropping. Right away I thought- mucus plug! I told her to immediately ambubag the patient. I rushed to PrH1. I gave 10 mg IV Dexamethasone (a steroid in order to minimize epiclottic, glottic, and upper tracheal swelling), prepared a suction machine, and a laryngoscope and ETTs in case a reintubation is necessary, and then I pulled out 26M's ETT. The ETT was almost totally blocked by several bloody mucus plugs.

26M was already awake, and he tolerated the ETT pull out well. I placed him on O2 via nasal cannula. When I left, his pulse oximeter showed a steady O2 sat of 92.

Entry 3.

After the close call on 26M, later in the night I went to CiH in order to operate on 9M, a boy who fell down a basketball court and hit his head on the floor a week ago. He has a 60 cc epidural hematoma on his left parietal area. When I arrived he was awake and was asking for food. I decided to cancel the operation. In about two months the EDH would be absorbed even without an operation. I don't like opening skulls if there is no clear indication for doing so, or if the patient is clinically improving.

Premium Chessgames Member
  visayanbraindoctor: 8 April 2015. <22 March 2015. Entry 1. Just before midnight, a Pulmonologist called me to PrH2 ER. He had come across a group of Catholic priests that he knew and that were bringing in an unconscious deacon who had fallen off a motorcycle.>

I am discharging 35M, the patient referred to above. He was co-managed with a Neurologist who convinced the family a post-op CT scan was necessary, even though I had told her and the family it was not needed at all, due to the fact that the patient was improving post-op and had not shown signs of permanent Neurological deficits.

For me, such post-op CT scans do not help me and do not make me change my management in a clinically improving patient. I only do them if I feel there is a complication going on in the brain and the patient may need to be operated on again. Otherwise, they just waste the family's funds.

As expected, the post-op CT scan showed no more hematomas that need to be operated on, just a contused brain. I knew this already because I had personally opened up the brain and removed these hematomas; and if the patient was improving, then there is probably no rebleed. Sometimes such CT scans would show some residual intra-cranial hematoma, but in view of a clinically improving patient, I never operate on these; they get absorbed and disappear usually within 2 weeks.

Premium Chessgames Member
  visayanbraindoctor: 11 April 2015. Entry 1. I debrided and repaired a frontal left scalp avulsion of 19M, a MF victim, in CiH ward under LA, bedside. Scheduling these cases in the OR is a a lot of hassle.
Premium Chessgames Member
  visayanbraindoctor: 12 April 2015.

Entry 1. I did another debridement and repair, bedside under LA, this time the lacerated left pinna (ear) of MF victim 53M in in PrH1.

Entry 2. To operate or not? A child 5M was hit by a motorcycle and had sustained a closed depressed fracture on the left temporo-parietal bone. He has a small 20 cc epidural hematoma but is awake, and so there is no indication to operate on him for the EDH. Since the fracture is completely covered by intact skin (a close fracture), there is little chance for it to become infected; and so a debridement and cleaning operation is not necessary either.

One can opt not to operate on these cases. However, CT scan showed that a piece of the depressed bone was penetrating into the brain. In such cases, especially for kids, I usually operate, removing the depressed bone. As a child grows, the bone may get pushed deeper into the brain, and you place the patient at risk later in life for seizures and Neuro deficits.

So I advised the anxious parents an operation, and they agreed. (Left temporal-parietal craniectomy, evacuation of epidural hematoma 4/12/15 4:16pm - 4:44 pm. Minimal blood loss, no blood transfusion required.) I threw away the depressed bone that I had removed. It was pretty small and for children, the bone usually just grows back. The new bone properly covers the brain and does not stab deeper into it.

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  visayanbraindoctor: 13 April 2015. I returned the left temporo-fronto-parietal bone of 30F, whom I had operated on 12 September 2014 for an acute subdural hematoma. She was on a tricycle that got hit by a ten wheeler truck.

(Replacement of bone left temporo-fronto-parietal 4-13-15 10:03 - 10:31 am)

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  visayanbraindoctor: 14 April 2015.

<2 April 2015. In PrH1, the Neurologist had referred 64F yesterday specifically for a tube ventriculostomy. 64F has a ruptured ACOM aneurysm. (Right frontal tube ventriculostomy, evacuation of CSF and intraventricular hemorrhage 4/2/15 3:20 to 3:48 pm.)>

I did a tracheostomy on 64F. Attempts to wean her off the ventilator had failed. (Tracheostomy 4-14-15, 10:08 - 10:20 pm.)

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  visayanbraindoctor: 16 April 2015.

I discharged the following post-op patients. They're doing fine.

<12 April 2015. A child 5M was hit by a motorcycle (Left temporal-parietal craniectomy, evacuation of epidural hematoma 4/12/15 4:16pm - 4:44 pm. Minimal blood loss, no blood transfusion required.)>

<13 April 2015. I returned the left temporo-fronto-parietal bone of 30F, whom I had operated on 12 September 2014 for an acute subdural hematoma. She was on a tricycle that got hit by a ten wheeler truck. (Replacement of bone left temporo-fronto-parietal 4-13-15 10:03 - 10:31 am)>

Premium Chessgames Member
  visayanbraindoctor: 17 April 2015.

<2 April 2015. 26M, a MF victim. (Left parietal-frontal craniectomy, evacuation of intracerebral hematoma, bone transplant to left hemiabdomen SQ layer 4/2/15 8:55 to 10:21 pm.)>

Five days ago 26M, already awake, began to develop a fever of 39 to 40 C. That got me worried, was he developing a CNS infection? He had sustained a depressed fracture and I could not totally rule out some bacteria getting into his meninges or brain. I did a CT scan but it showed no abscess or empyema. Clinically he was awake, no complain of headache, and that led me to rule out meningitis or other CNS infections. CNS infections almost invariably lower a patient's sensorium.

Another possible source: I noticed that that the IV site on his right hand and forearm had developed thrombo-phlebitis. The veins had clotted to a dark blue and the skin was swollen. I had the IV pulled out.

Three days ago, 26M still had fever, at around 38 to 39. His brain injury had left him paralyzed on his right extremities, and this seemed to have been aggravating his thrombo-phlebitis. I have had patients with this condition that began throwing emboli into their lungs, killing them. I had anti-embolic stockings placed on his right lower extremity.

Two days ago 26M's fever had gone down to below 38.

Yesterday, 26M's fever was gone. (What a relief for me.)

Today I discharged 26M. No fever. He still had right hemiparesis and verbal dysphasia stemming from his brain injury, but at least he's alive, and may still possibly regain some of his motor strength and speech back.

Apr-18-15  iking: doc <VBD> .. such a lovely diary...maybe someday, maka-uli ikaw di sa Iloilo and visit the old Airport in Mandurriao ...
Apr-19-15  SugarDom: He never said he's from Iloilo <iking>, and it's very important that VBD remains anonymous because of this forum which he intended to be experimental in the first place. I understand that now.
Premium Chessgames Member
  visayanbraindoctor: <sugardom> Yes I would rather stay anonymous.

<iking: such a lovely diary> Maayo man nga nanamian ka sa 'diary'. Mayad man nga nanamian kaw sa 'diary'. It's an experimental one, as the rules above announce.

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  visayanbraindoctor: 18 April 2015. About 10:30 pm.

We often see multiple vehicles pile-up accidents in the movies, but it's rare in real life. Nevertheless, one just occurred in front of PrH1.

An SUV driven by a drunk hit a tricycle, and on top of them a motorcycle landed.

I had to intubate the comatose driver of the motorcycle 30M. The ER Resident Physician on Duty could not do it; it turned out he had artificial teeth which I removed first. He is in a very bad way and probably won't make it.

Premium Chessgames Member
  visayanbraindoctor: 19 April 2015.

Entry 1.

<2 April 2015. Entry 1. In PrH1, the Neurologist had referred 64F yesterday specifically for a tube ventriculostomy. 64F has a ruptured ACOM aneurysm. (Right frontal tube ventriculostomy, evacuation of CSF and intraventricular hemorrhage 4/2/15 3:20 to 3:48 pm.)>

<I did a tracheostomy on 64F. Attempts to wean her off the ventilator had failed. (Tracheostomy 4-14-15, 10:08 - 10:20 pm.)>

I had pulled out the tube ventriculostomy after a week. 64F still could not be weaned off, possibly because she remained drowsy. Repeat CT scan still showed hydrocephalus. The Neurologist, Pulmonologist, and I decided that the best option was to place in a permanent ventriculo peritoneal shunt.

I hate these things because they are foreign bodies and are prone to infections and all kinds of complications, but I went along with the consensus. (Ventriculo-peritoneal shunting 4-19-15, 7:20 - 8:14 pm.)

Entry 2. Right after the above I had to go to CiH and operate on a comatose anisocoric MF victim 52M. He probably won't make it but his family was insistent on aggressive measures. (Right parietal-temporal craniectomy, evacuation of acute subdural hematoma, bone transplant to left hemiabdomen SQ layer 4/19/15 10:36 to 11:35 pm. Tracheostomy 4/19/15 11:42 to 11:51 pm. Minimal blood loss, no BT required.)

Premium Chessgames Member
  visayanbraindoctor: 20 April 2015.

<18 April 2015. About 10:30 pm.

An SUV driven by a drunk hit a tricycle, and on top of them a motorcycle landed.

I had to intubate the comatose driver of the motorcycle 30M.>

There was a delay because of financial reasons. 30M was intubated in PrH1, then got transferred to PrH2, then was transferred again to the public CiH. Right after 52M, I operated on 30M on the same operating room. My Anesthesiologist and I, and the OR nurses I did not even leave the OR. 30M was decorticate pre-op and probably won't survive, as with many such severely brain injured patients.

(Left and right frontal craniectomies, evacuation of acute subdural hematomas, bone transplant to left hemiabdomen SQ layer 4/20/15 1:14 to 2:32 am. Tracheostomy 4/20/15 2:42 to 2:59 am. Minimal blood loss, no BT required.)

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