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visayanbraindoctor
Member since Jun-04-08 · Last seen Mar-26-15
Good Day to All! Ma-ayong adlaw sa tanan. And my thanks to CG.com for this excellent website. Salamat CG.com. 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 intubation—called 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.

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Chessgames.com Full Member

   visayanbraindoctor has kibitzed 7148 times to chessgames   [more...]
   Mar-26-15 twinlark chessforum
 
...
 
   Mar-23-15 visayanbraindoctor chessforum
 
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 ...
 
   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.
 
   Feb-10-15 Keres vs Bogoljubov, 1936 (replies)
 
visayanbraindoctor: <Honza Cervenka: 32.Bc1 is lovely as well.> Keres was one dynamite tactician. 32. Bc1 is the kind of move the vast majority of chess players would not even consider in their list of options. Keres probably had already seen it when moving 30. Qh5. Normally humans ...
 
(replies) indicates a reply to the comment.

Kibitzer's Corner
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Mar-04-15
Premium Chessgames Member
  visayanbraindoctor: 1 March 2015. I operated on 21M, GCS 7, with a huge 70 cc right parietal epidural hematoma. (Operating time 6:54 - 7:41 pm) Some one had hit his head with a rock. He was not aspirated. As typical in such pure EDH cases, 21M woke up after the operation. I like these kinds of operations.
Mar-04-15
Premium Chessgames Member
  visayanbraindoctor: 2 March 2015. In CiH, I removed the left hemisphere acute subdural hematoma of 73M, who was hit by a motorcycle while he was walking. He is GCS 7, comatose, and severely aspirated. I also did a tracheostomy in order to facilitate suctioning of pulmonary secretions. (Operating time 2:49 - 3:45 pm)

Nevertheless, in such cases of severely aspirated septuagenarians, one can't expect them to survive the ensuing pneumonia-sepsis roller coaster ride.

Mar-04-15
Premium Chessgames Member
  visayanbraindoctor: 3 March 2015. Entry 1. At witching hour, I was called to Prh1 ER. The ROD informed me that there was a head injured MF patient with BP 30 palpatory, yet the patient was communicative. I told her to look for other injuries; the cause for such a drop in BP is usually blood loss. After a few minutes, she called back saying the patient also had his bones jutting out of his forearm, and that he had a scalp avulsion. So that's where the blood loss came from.

I immediately ordered over the phone to fast drip 200cc of NSS or Plain LR, and 500cc of Voluvent blood replacement fluid, and then rushed off to the ER. When I arrived, the BP had climbed back to 100 systolic. The CT scan showed a normal brain. Shortly after, the BP rose to 120/80, with HR 80 per minute.

I told the worried wife that the crisis is over. I proceeded to debride and suture the huge left parietal-temporal scalp avulsion under LA in the ER as VS had already stabilized.

They will probably transfer to the public CiH tomorrow because of lack of funds.

Entry 2. I operated on another left basal ganglia hypertensive hemorrhagic stroke, just barely a week after I did <23 February 2015. Entry 1. Operated on 46M, GCS 7, huge left basal ganglia hypertensive hemorrhagic stroke>, 36M a GCS 7 patient.

36M already had a 40 degree fever pre-op from his pneumonia, and I also did a tracheostomy on him.

(Operating time 2:38 - 4:28 pm)

Comatose basal ganglia hemorrhagic strokes with severe pneumonia always carries a poor prognosis, especially in a public hospital with no reliable mechanical ventilator.

Mar-05-15
Premium Chessgames Member
  visayanbraindoctor: 4 March 2015. Entry 1. <3 March 2015. At witching hour, I was called to Prh1 ER. The ROD informed me that there was a head injured MF patient with BP 30 palpatory, yet the patient was communicative.> Having stabilized, the wife decided to transfer the patient back to the public hospital in their province adjacent to mine.

Entry 2. <3 March 2015.. I operated on another left basal ganglia hypertensive hemorrhagic stroke, just barely a week after I did <23 February 2015. Entry 1. Operated on 46M, GCS 7, huge left basal ganglia hypertensive hemorrhagic stroke>, 36M a GCS 7 patient.> 36M died of pneumonia and septic shock, same as 46M a week before him.

Entry 3. At dawn I was called to CiH. Two patients were referred for severe respiratory distress.

The first was MF victim 40M, a complete cervical spinal cord transection C4 level. In other words, his spinal cord in his neck was severed, thus compromising his respiratory efforts. By the time I arrived, he was in CP arrest and was pronounced dead shortly after.

40M's only watcher was his small son, about 10 years old. The boy was crying at bedside all throughout the resuscitation efforts in the ward.

The second was 58M, another MF victim. Blood and mucus was clogging up his trachea, and I intubated him in the nick of time, but he remained comatose afterwards, GCS 6.

Entry 4. At dusk, a comatose girl, 11F, arrived in PrH2 ER, having been hit by a car. She had a small right temporo-parietal epidural hematoma and on the contralateral side a small left thalamic hemorrhage. Since her entire brain was also swollen, I decided to do a wide craniectomy on the site with the epidural hematoma and transplant the bone to her left hemiabdomen subcutaneous layer. (Operating time 6:58 – 7:32 pm.)

Nothing much I can do about the thalamic hemorrhage. The thalamus is part of the diencephalon, through which the ascending reticular activating system runs, the structure said to be the basis for consciousness and wakefulness. If there is a severe primary injury to her thalamus 11F will probably remain comatose for quite some time post-op, .

Entry 5. Later in the night, I did a tube ventriculostomy and tracheostomy on MF victim 58M in CiH, the same patient I intubated above as described in entry 3. (Operating time 10:29 – 11:19 pm.) He had incurred a massive intraventricular bleed, which in turn blocked the CSF flow through his ventricles thus causing communicating hydrocephalus. CSF, of which the brain produces half a liter a day, can’t flow and get absorbed properly and was thus increasing the intracranial pressure.

Mar-07-15
Premium Chessgames Member
  visayanbraindoctor: 7 March 2015. Entry 1. Just after midnight, I operated on an MF victim, 34M. (Evacuation of a 60 cc right parietal-occipital epidural hematoma and bone transplant to his left hemi-abdomen SQ. Operating time 1:10 -2:30am.) The patient had arrived in PrH 2 ER just before midnight, and was comatose GCS 6 and anisocoric. Fortunately, the family had the funds to pay the downpayment for an immediate operation in a private hospital. I intubated the patient in the ER and directly admitted him into the OR.

I had unexpected problems with bleeding. Sometimes you get patients who are oozers and bleeders. There is no active bleeding upon closure but the incision lines and needle-suture puncture wounds tend to ooze blood. In these patients I automatically assume some kind of bleeding problem and continue giving Vitamin K and Tranexamic acid post-op. (I routinely give these meds pre-op.) Many of these patients are alcoholic or have liver or kidney problems.

I had rushed him to the OR without blood since he was in the process of brain herniation, and so I had to make certain bleeding was kept to a minimum- injecting NSS and epinephrine on the surgical site, tacking the dura, suturing all actively bleeding scalp arteries. I did all of these, yet there was still some oozing, which clogged my epidural drain.

Better safe than sorry. I reopened the scalp and checked for active bleeders. There was none. Subsequently, I removed the blocked drain and placed two new ones to be safe, one epidural and one subgaleal.

Post-op around 12 hours later, 34M pulled out his ETT. Good. Patients who have regained sufficient wakefulness to self extubate usually survive.

Entry 2. <4 March 2015. Entry 5. Later in the night, I did a tube ventriculostomy and tracheostomy on MF victim 58M in CiH>

58M died suddenly of pulmonary problems in this afternoon; despite the fact that he had already woken up two days post-op. His relatives were ambubagging him in the ward. I suspect one of his relatives might have pushed in air too forcibly as he was breathing out, thus rupturing the lungs. Unfortunately there is no reliable mechanical ventilator in the public CiH, and I have such high mortality rates on patients that are being ambubagged manually by untrained relatives.

Mar-07-15  Transformer: <I suspect one of his relatives might have pushed in air too forcibly as he was breathing out, thus rupturing the lungs.>

Just curious, did you inform the relatives of your suspicion?

Mar-09-15
Premium Chessgames Member
  visayanbraindoctor: <Transformer: <I suspect one of his relatives might have pushed in air too forcibly as he was breathing out, thus rupturing the lungs.>

Just curious, did you inform the relatives of your suspicion?>

No. It serves no constructive purpose after the death of the patient. The fundamental fault is institutional anyway; the public hospital lacks a mechanical ventilator.

Mar-09-15
Premium Chessgames Member
  visayanbraindoctor: 9 March 2015. Entry 1. I operated on 15M, who a week ago on 2 March 2015 got hit on the head by a piece of iron equipment in a mining quarry. (Left temporo-fronto-parietal craniectomy, evacuation of epidural hematoma and intracerberal contusion-hematoma, dura repair with temporalis muscle flap, bone transplant to left hemi-abdomen SQ layer. Operating time 11:53 am - 12:59 pm).

Although the intracranial hematomas were small and not exerting life-threatening pressure, it was an open fracture, and I should have operated days ago; but it's only now that the family was able to secure OR needs, thanks to the boy's master aiding them financially (I must say a rather delayed aid).

Thus far there are no signs of CNS infection, which sometimes occurs in open skull fractures.

Entry 2.

<20 February 2015. Entry 2. Operation 2. This one I did in the public CiH, 25M who fell off a motorcycle, GCS 7. He has a large right frontal epidural hematoma. Usually these patients awake post-op, but 25M also had severely aspirated. I also did a tracheostomy on him. he is young and so I am hopeful he will survive his pneumonia.>

25M is still alive. Two days ago I pulled out his tracheostomy tube. Today I transferred him from the CiH ICU to the ward.

Mar-09-15  GreenLantern: <No. It serves no constructive purpose after the death of the patient.>

I thought so - definitely more compassionate not to do so. Thanks.

Mar-10-15
Premium Chessgames Member
  visayanbraindoctor: 10 March 2015. Entry 1. Last night, five family members were riding on a single motorcycle- father, mother, their two children, and father's sister. They hit another motorcycle. Father and the younger child died. I admitted the remaining child 7F to CiH near midnight.

The stuporous (GCS 9) 7F had a deeply depressed closed right occipital fracture with underlying epidural hematoma and cerebral hemorrhagic contusion. She also had a left radio-ulna fracture and a right distal femoral fracture which had resulted in significant blood loss. In femoral fractures, a patient can lose more than a liter of blood, but since it seeps into the huge thigh soft tissue compartment, it may not be clearly visible to the layman, and shows only as thigh swelling. 7F had incurred significant blood loss.

It took the family the rest of today to secure OR needs and blood, but I finally got to operate on 7F. (Right occipital craniectomy, evacuation of epidural hematoma, bone transplant to left hemiabdomen subcutaneous layer 3/10/15 9:25 - 10:10 pm. I trepanned and sawed around the depressed bone and lifted it whole, but avoided removing the medial part of it adjacent to the sagittal sinus where there was a dried blood clot plugging the area. Neither did I remove this small blood clot. I did not want any unnecessary additional bleeding from the sinus, the brain's major draining vein.)

Mar-14-15
Premium Chessgames Member
  visayanbraindoctor: 12 March 2015. Entry 1. An old woman 80F was found lying beside the highway, a hit and run victim. She arrived in PrH2 ER with HR 62 but BP 0, and died shortly after intubation. In the local setting this is considered and ER death and not formally admitted; although it's registered in a medico-legal logbook in the ER.

Entry 2. Later that evening, another senior citizen 76M, anisocoric and comatose (GCS 6) and was referred to me in PrH1 by a Neurologist. The Oracle showed that he had a massive chronic subdural hematoma on his right hemisphere and a smaller one on the left hemisphere.

The CSDH is regarded as a traumatic injury, but doesn't present itself that way. Instead it may insidiously present as a steady lowering of sensorium over a range of weeks or months in the elderly or the alcoholic. And then the patient can suddenly deteriorate fast as terminal brain herniation occurs, in which case the signs and symptoms are indistinguishable clinically from a sudden stroke.

That's why if you have an elderly relative or an alcoholic friend who begins to show signs of sensorial changes (laymen would often say that he is weaker, is recently talking in a nonsensical manner or just talks less, sleeping more of the time, mumbling and stumbling about), it's probably best to have a CT scan done on him.

I transferred 76M to the public CiH because of financial reasons, after conferring with and asking permission from the admitting Neurologist. I have rarely ever seen an anisocoric comatose septuagenarian survive in a public hospital with no mechanical ventilator, and even if you operate on them they soon enter the pneumonia-sepsis roller coaster ride and usually fall off the first turn.

Mar-14-15
Premium Chessgames Member
  visayanbraindoctor: 14 March 2015. Entry 1.

<12 March 2015. Later that evening, another senior citizen 76M, anisocoric and comatose (GCS 6)>

76M died of septic shock and pneumonia in CiH. His son had decided not to push through with an operation after I advised him it most probably would not benefit the patient anyway, as he already had pneumonia and sepsis (I usually describe pneumonia and sepsis as germs from the lungs entering and poisoning the blood to the local folks here as they can't grasp the technical description well. "Ang kagaw sa baga nagsulod na sa dugo ug gihiloan ang pasyente", in Sugbuanon Visayan.) Or another way of putting it is that he decided he could not afford to spend more money for the OR needs. As a policy I inform the relatives of poor prognosis especially since most of the the people here are impoverished. I don't want them to spend unnecessarily.

Mar-14-15
Premium Chessgames Member
  Annie K.: <Doc> I'm curious... sepsis usually results from pneumonia in your cases; I know it can also result from infected wounds. What else can cause it, and does it have its own symptoms?
Mar-18-15
Premium Chessgames Member
  visayanbraindoctor: <Annie K.: <Doc> I'm curious... sepsis usually results from pneumonia in your cases; I know it can also result from infected wounds. What else can cause it, and does it have its own symptoms?>

Sepsis is a general term used to refer to a condition wherein the whole body 'inflames' as a reaction to some infection. Every several years, some physician's organization comes up with various classification criteria and definitions. In reality, it is a gradation of signs and symptoms that occur as bacterial infection spreads to the bloodstream, begins to affect all organ-systems, and the body then responds. Uncontrolled, it always ends in septic shock. The body loses its control of its blood vessels and these naturally dilate, thus the effective blood volume increases, thus the blood pressure lowers, all the way to zero eventually.

If something irritates your skin, it naturally inflames as the body releases inflammatory substances as a response. Classically, you get the signs of calor rubor tumor dolor (warmth, redness, swelling, pain on your skin). How do you get these signs and symptoms? Your blood vessels in the affected skin dilate.

Now to sepsis. Think of such an inflammatory response occurring as a reaction to bacteria getting into your bloodstream, meaning your entire body.

Almost any uncontrolled bacterial infection can cause it. You mention two above, pneumonia and infected wounds.

Example 3: When I was a medical student, I rotated in the OB-Gyne Department. In the Philippines abortion is illegal, a crime by law. Many unwanted pregnancies result in the women (usually the impoverished ones) going to quack abortionists. These abortionists insert unsterilized Foley catheters or other tubes inside the preggy's uterus. The fetus dies, but outside bacteria also gets introduced into the uterus. The bacteria (invariably numerous species) multiplies and thrives on the dead decaying fetus. Some begin crossing into the bloodstream. Sepsis. The woman (many are actually teenage girls) often come to the ER with fever, tachycardia, tachypnea, lowered sensorium.

Example 4: In my setting many of the local eateries don't clean or heat their utensils well. Now and then, one of my acquaintances (including me) gets sick with gastrointestinal discomfort. If fever also occurs, I get worried. Typhoid (Salmonella) is widespread hereabouts.

Typically you get a patient eating in local eateries. She begins to have fever. In the next few days she becomes so weak she can't get off her bed, and the fever reaches 40 degrees. She has sepsis, originating from a specific bacteria Salmonella.

Hope the above examples help.

Mar-18-15
Premium Chessgames Member
  visayanbraindoctor: 18 March 2015. Yesterday, Medicine Department in CiH referred a comatose 52M to me. They had a CT scan done that showed a huge (60cc) right basal ganglia hemorrhage.

Approximately 60% of hypertensive hemorrhagic strokes occur in the basal ganglia part of the deep gray matter in the telencephalon (deep beneath our cerebral hemisphere). I have already done two operations this past month, both dying from pneumonia and sepsis shortly after the operation.

52M is typical. Comatose, he can't cough out his secretions. Pneumonia is beginning (increased respiratory rate, slight fever, rales, suprasternal notch retraction). When I first saw him yesterday, I immediately injected Diazepam for pre procedural sedation and intubated him. His epiglottis was severely swollen and I could not get even an ETT 7.5 inside. Usual ETT for adults is 7.5 to 8.5. Turned out that the internist had already tried intubating him and failed, and in so doing probably traumatized the windpipe's opening causing the swelling. I finally got an ETT size 7 in.

The family decided on an aggressive course. They secured the necessary materials by early morning today and so I proceeded to operate. (Right fronto-temporo-parietal craniectomy, frontal cortisectomy, evacuation of basal ganglia hemorrhage, bone transplant to left hemiabdomen subcutaneous layer, tracheostomy 3-18-15 9:50 to 11:34 am.)

As usual in such cases, I did a wide craniectomy so as to allow the still swelling brain more space to expand to. The bone I keep in the patient's left abdominal subcutaneous layer, in order to return after 6 months if he survives. (In other institutions, they throw away the bone and place titanium plate and bone cement on the skull defect eventually, or they keep the bone in a bone bank. Titanium plates are too expensive for my patients here, and I don't feel comfortable placing a loadful of extraneous bone cement permanently into my patients' skull.) I approached via a cortisectomy in the frontal lobe anterior to the motor cortex. I don't want to damage this important cortical gyrus that controls volitional movement, but this probably won't matter as he is already half paralyzed on his left extremities. The general rule is that whatever paralysis is present pre-op is also present post-op, and the treatment purpose is to save the patient's life, not necessarily the motor function of a limb. Also according to my own SOP, I did a tracheostomy, in order to increase his survival chances in the face of pneumonia.

Mar-19-15
Premium Chessgames Member
  Annie K.: Much thanks doc, very helpful explanation!

The details about bone replacement always interest me too. :)

Another question please, why does the brain produce so much CSF?

Mar-20-15
Premium Chessgames Member
  WannaBe: Just want to share this:

http://www.freep.com/story/news/nat...

Mar-20-15
Premium Chessgames Member
  visayanbraindoctor: <WannaBe> Thank you. That's so touching. It usually happens when you lose a child or teenager that could have been saved had the circumstances been just slightly different.
Mar-20-15
Premium Chessgames Member
  visayanbraindoctor: <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.

In case you use the original craniectomized bone, you just fit it back into the hole in the skull. If the bone isn't beveled, you wire it to the adjacent bone. (You drill small holes on the returned bone and the adjacent bones and tie the returned bone to the adjacent bones with wire through these holes.) I don't have to do this because I always make sure that the bone I remove is beveled. The beveled edges allow it to fit in immovably, and then I just place sutures on the temporalis muscle and periosteum on top of it and crisscrossing it, holding it in place.

<Another question please, why does the brain produce so much CSF?>

IMO it follows a general phenomenon in the body. The fluid in any compartment of our body always gets constantly replaced. Whether it's the CSF, peritoneal fluid, lymph, blood, etc..

In other words the volume of a fluid in a body compartment is always in equilibrium, meaning fluid always gets in and fluid always gets out. The fluid does not stagnate.

If you're asking why is this so, I would opine that it has something to do with the body's defenses against pathogens. If bacteria gets into a compartment of the body where the fluid is stagnant, not being replaced, it could well multiply without hindrance. Not sure, but that sounds reasonable to me.

Mar-22-15
Premium Chessgames Member
  visayanbraindoctor: 21 March 2015. Entry 1. CiH Medicine Department referred a stuporous CVA case yesterday. Blind since birth, this patient works as a blind masseur. These remarkable people, although disabled since birth, are still able to find work.

Unfortunately he has suffered from a large left basal ganglia hypertensive hemorrhage. Unlike right sided ones such as ('18 March 2015. Yesterday, Medicine Department in CiH referred a comatose 52M to me. They had a CT scan done that showed a huge (60cc) right basal ganglia hemorrhage'), this carries a poorer prognosis because the left hemisphere is usually the dominant one, and so even if he survives, he will not only have right sided weakness, but will also have impaired speech.

The patient's family and employee were cooperative and managed to procure the necessary OR needs and blood by morning today. So I proceeded with the operation. (Left fronto-temporo-parietal craniectomy, frontal cortisectomy, evacuation of basal ganglia hemorrhage, bone transplant to left hemiabdomen subcutaneous layer, tracheostomy 3-21-15 2:15 to 4:26 pm.) I thought that his pulmonary status was alright at first but my Anesthesiologist found out he had lots of secretions upon intubation, and so I also proceeded with a tracheostomy.

Mar-22-15
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.)

Mar-22-15
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

Mar-22-15
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.

Mar-23-15
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.

Mar-23-15
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.

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